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True Facts About FlavonoidsFlavonoids and arthritis -
Oxymatrine prevents synovial inflammation and migration via blocking NF-κB activation in rheumatoid fibroblast-like synoviocytes. Ma A, Yang Y, Wang Q, Wang Y, Wen J, Zhang Y. Anti-inflammatory effects of oxymatrine on rheumatoid arthritis in rats via regulating the imbalance between Treg and Th17 cells.
Mol Med Rep. Wen HL, Yang G, Dong QR. Ellipticine inhibits the proliferation and induces apoptosis in rheumatoid arthritis fibroblast-like synoviocytes via the STAT3 pathway. Immunopharmacol Immunotoxicol.
Zhao YC, Xue CH, Zhang TT, Wang YM. Saponins from Sea Cucumber and Their Biological Activities. He Y, Hu Z, Li A, Zhu Z, Yang N, Ying Z, et al. Recent advances in biotransformation of saponins. Ma X, Chen G, Wang J, Xu J, Zhao F, Hu M, et al. Pedunculoside attenuates pathological phenotypes of fibroblast-like synoviocytes and protects against collagen-induced arthritis.
Scand J Rheumatol. Yu WG, Shen Y, Wu JZ, Gao YB, Zhang LX. Madecassoside impedes invasion of rheumatoid fibroblast-like synoviocyte from adjuvant arthritis rats via inhibition of NF-κB-mediated matrix metalloproteinase expression.
Chin J Nat Med. Kwon OG, Ku SK, An HD, Lee YJ. Evidence-based Complement Altern Med. Guo Y, Xing E, Liang X, Song H, Dong W. Effects of total saponins from Rhizoma Dioscoreae Nipponicae on expression of vascular endothelial growth factor and angiopoietin-2 and Tie-2 receptors in the synovium of rats with rheumatoid arthritis.
J Chinese Med Assoc. Liu C, Yang Y, Sun D, Wang C, Wang H, Jia S, et al. Abbreviated title: 16 :1— Liu Y, Li M, He Q, Yang X, Ruan F, Sun G. Periploca forrestii saponin ameliorates murine CFA-induced arthritis by suppressing cytokine production.
Mediators Inflamm. Javadi F, Ahmadzadeh A, Eghtesadi S, Aryaeian N, Zabihiyeganeh M, Rahimi Foroushani A, et al. The Effect of Quercetin on Inflammatory Factors and Clinical Symptoms in Women with Rheumatoid Arthritis: A Double-Blind, Randomized Controlled Trial.
J Am Coll Nutr. Ahmad S, Alam K, Hossain MM, Fatima M, Firdaus F, Zafeer MF, et al. Anti-arthritogenic and cardioprotective action of hesperidin and daidzein in collagen-induced rheumatoid arthritis.
Mol Cell Biochem. Jiang CP, He X, Yang XL, Zhang SL, Li H, Song ZJ, et al. Anti-rheumatoid arthritic activity of flavonoids from Daphne genkwa.
Sun Y wen, Bao Y, Yu H, Chen Q, jing, Lu F, Zhai S, et al. Anti-rheumatoid arthritis effects of flavonoids from Daphne genkwa. Chi L, Gao W, Shu X, Lu X.
A natural flavonoid glucoside, icariin, regulates th17 and alleviates rheumatoid arthritis in a murine model. Zhai KF, Duan H, Cui CY, Cao YY, Si JL, Yang HJ, et al. Liquiritin from Glycyrrhiza uralensis Attenuating Rheumatoid Arthritis via Reducing Inflammation, Suppressing Angiogenesis, and Inhibiting MAPK Signaling Pathway.
Wang X, He X, Zhang CF, Guo CR, Wang CZ, Yuan CS. Anti-arthritic effect of berberine on adjuvant-induced rheumatoid arthritis in rats. Shan L, Tong L, Hang L, Fan H. Fangchinoline supplementation attenuates inflammatory markers in experimental rheumatoid arthritis-induced rats. Total saponin from Anemone flaccida Fr.
Schmidt prevents bone destruction in experimental rheumatoid arthritis via inhibiting osteoclastogenesis. Rejuvenation Res. Epub Sep Liang XJ, Guo YC, Sun TY, Song HR, Gao YX.
Anti-angiogenic effect of total saponins of Rhizoma Dioscorea nipponica on collagen induced-arthritis in rats. Exp Ther Med. Download references. The authors are thankful to Biodiversity and Biotechnology Network of the Legal Amazon, Graduate Program in Health Sciences - Federal University of Maranhão and Graduate Program in Microbial Biology - CEUMA University for providing all the necessary facilities related to the present work.
Biodiversity and Biotechnology Network of the Legal Amazon, University of Maranhão - BIONORTE, State University of Maranhão— UEMA, Maranhão, São Luís, Brazil.
Graduate Program in Health Sciences, Federal University of Maranhão - UFMA, Maranhão, São Luís, Brazil. Graduate Program in Microbial Biology, CEUMA University - UniCEUMA, Maranhão, São Luís, Brazil. Santa Terezinha College - CEST, Maranhão, São Luís, Brazil. Veterinary Medicine Course, Maurício de Nassau College - UNINASSAU, Maranhão, São Luís, Brazil.
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A literature review. Clin Phytosci 7 , 58 Download citation. Received : 11 January Accepted : 01 June Published : 24 June Anyone you share the following link with will be able to read this content:.
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A literature review Luis Ângelo Macedo Santiago 1 , Roberval Nascimento Moraes Neto 2 , Ana Caroline Santos Ataíde 2 , Dâmaris Cristina Sousa Carvalho Fonseca 3 , Enio Fernandes Aragão Soares 4 , Joicy Cortez de Sá Sousa 3 , Renata Mondego-Oliveira 5 , Rachel Melo Ribeiro 2 , Maria do Socorro de Sousa Cartágenes 2 , Lídio Gonçalves Lima-Neto 3 , Rafael Cardoso Carvalho ORCID: orcid.
Abstract Rheumatoid arthritis RA is a systemic inflammatory disease characterized by synovial inflammation leading to progressive joint erosion and, eventually, joint deformities. An extensive literature survey was undertaken through different online platforms: PubMed, SciELO, and Virtual Health Library databases, to identify phytochemical compounds used in RA treatment and the descriptors used were medicinal plants, herbal medicines, and rheumatoid arthritis.
Introduction Rheumatoid arthritis RA is a systemic inflammatory disease characterized by symmetrical arthritis and synovial inflammation, progressive joint erosion, and, eventually, joint deformities.
Methodology Substantial literature survey was undertaken to abridge the phytochemical compounds in the treatment of rheumatoid arthritis and its therapeutic properties. Immunopathology of rheumatoid arthritis Although the etiology of RA is not clarified, it is possible to affirm that the disease results from the action of autoreactive T and B cells.
Table 1 Cytokines and their role in the immunopathogenesis of Rheumatoid Arthritis Full size table.
Table 2 Phytochemicals used in the treatment of rheumatoid arthritis Full size table. Full size image. Conclusion and future directions Conventional RA treatment produces mixed results: some cause undesirable side effects, while others can worsen the disease.
Availability of data and materials Not applicable. References Firestein GS. Article CAS Google Scholar Jung SM, Lee J, Baek SY, Lee J, Jang SG, Hong SM, et al. Article Google Scholar Burmester GR, Pope JE. Article CAS Google Scholar Yang Y, Zhang X, Xu M, Wu X, Zhao F, Zhao C.
Article CAS Google Scholar Liu W, Zhang Y, Zhu W, Ma C, Ruan J, Long H, et al. Article Google Scholar Lee CJ, Moon SJ, Jeong JH, Lee S, Lee MH, Yoo SM, et al. Article CAS Google Scholar Yap H-Y, Tee S, Wong M, Chow S-K, Peh S-C, Teow S-Y.
Article CAS Google Scholar Firestein GS, McInnes IB. CAS PubMed Google Scholar Wang N, Zhao X, Huai J, Li Y, Cheng C, Bi K, et al. Article Google Scholar Tanaka T, Narazaki M, Kishimoto T. Article Google Scholar Luo C, Xu X, Wei X, Feng W, Huang H, Liu H, et al.
Article CAS Google Scholar Pu J, Fang FF, Li XQ, Shu ZH, Jiang YP, Han T, et al. Article CAS Google Scholar De Villiers A, Venter P, Pasch H. Article CAS Google Scholar Burda S, Oleszek W. Article CAS Google Scholar Cao G, Sofic E, Prior RL. Article CAS Google Scholar Li AN, Li S, Zhang YJ, Xu XR, Chen YM, Li H, Bin.
Article Google Scholar Saija A, Scalese M, Lanza M, Marzullo D, Bonina F, Castelli F. Article CAS Google Scholar Wang Y, Gao J, Xing LZ. Article Google Scholar Liu C, Yang S, Wang K, Bao X, Liu Y, Zhou S, et al.
Article CAS Google Scholar Golbahari S, Abtahi Froushani SM. Article CAS Google Scholar Yang J, Cai H, Da, Zeng YL, Chen ZH, Fang MH, Su YP, et al. Article CAS Google Scholar Liang J, Chang B, Huang M, Huang W, Ma W, Liu Y, et al. Article CAS Google Scholar Wen HL, Yang G, Dong QR. Article CAS Google Scholar Zhao YC, Xue CH, Zhang TT, Wang YM.
Article CAS Google Scholar He Y, Hu Z, Li A, Zhu Z, Yang N, Ying Z, et al. Article CAS Google Scholar Yu WG, Shen Y, Wu JZ, Gao YB, Zhang LX. Article CAS Google Scholar Ahmad S, Alam K, Hossain MM, Fatima M, Firdaus F, Zafeer MF, et al.
Article CAS Google Scholar Jiang CP, He X, Yang XL, Zhang SL, Li H, Song ZJ, et al. Article CAS Google Scholar Wang X, He X, Zhang CF, Guo CR, Wang CZ, Yuan CS.
Article CAS Google Scholar Liu C, Yang Y, Sun D, Wang C, Wang H, Jia S, et al. Article CAS Google Scholar Download references. Acknowledgements The authors are thankful to Biodiversity and Biotechnology Network of the Legal Amazon, Graduate Program in Health Sciences - Federal University of Maranhão and Graduate Program in Microbial Biology - CEUMA University for providing all the necessary facilities related to the present work.
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Competing interests There is no conflict of interest. In addition, isorhamnetin and morin also decrease ROS production, chondrocyte apoptosis, and the microenvironment in subchondral bone by inhibiting the NF-κB, MAPK, and AKT pathways 75 , 76 , Table 1 Figure 3.
Consistently, baicalin decreases the production of pro-inflammatory cytokines IL-6, IL-8, and TNFα, inactivates the NF-κB pathway, suppresses ECM degradation, and inhibits chondrocyte apoptosis , Table 1 Figure 3.
Flavocoxid, a medical food mainly containing two flavonoids, baicalin and catechins, exhibits protective effects by regulating the activity of arachidonic acid metabolism. It has been reported that scutellarin, chrysin, and nobiletin may inhibit TNFα-induced inflammatory cytokines and ECM catabolic factors and enhance aggrecan and collagen II production by suppressing the NF-κB signaling pathway 79 , 80 , Table 1 Figure 3.
Endoplasmic reticulum ER stress has been associated with the activation of inflammation by activating the NF-κB pathway Vitexin, an active compound from hawthorn leaf, has been demonstrated to inhibit ER stress, thereby inhibiting the NF-κB pathway and inflammatory responses Epigallocatechingallate EGCG , an active ingredient in green tea, has been linked to inflammation inhibition and cartilage degradation in OA.
Silibinin is one of the main active compounds in the fruits and seeds of Silybum marianum L. The maritime pine bark extract, Pycnogenol, has been standardized. Several clinical trials have been performed.
The clinical symptoms in the placebo group do not obviously change. In addition, Pycnogenol may decrease the dosage and frequency of NSAIDs or COX-2 inhibitors and reduce their adverse effects. Alpinetin, a flavonoid isolated from Alpinia katsumadai Hayata Zingiberaceae , has shown various biological effects, including anti-inflammatory.
Eriodictyol is often found in citrus fruits and has reported broad bioactivities. Similar results are also reached by naringenin, naringin, and pinocembrin 88 , , Table 1. Liquiritigenin is the main active compound from the rhizomes of Glycyrrhiza uralensis Fisch.
Bavachin has been screened for interrupting DNA-binding activity, and bavachin 1, 2. Similarly, hesperetin inhibits IL-1β-induced inflammatory responses and ECM degradation by suppressing NF-κB and stimulating the NRF2 pathway in primary human chondrocytes and DMM-induced mouse OA models The value of anthocyanins in protecting against the progression of OA and obesity has been comprehensively demonstrated Cyanidin, one of the main anthocyanins, has been reported to have anti-inflammatory activity.
The methanolic purple corn extracts are rich in cyanidinO-glucoside, pelargonidinO-glucoside, and peonidinO-glucoside. It has been demonstrated that purple corn extracts 6. The potential molecular mechanism might be associated with the inhibitory activity of anthocyanins in purple corn extracts against NF-κB and MAPK pathways , Genistein, a famous isoflavone in soybeans, has demonstrated anti-inflammatory and estrogen-like activities.
In collagenase-induced rat temporomandibular joint OA TMJOA models, genistein can significantly improve the histopathological changes, reduce the levels of IL-1β and TNFα, and inhibit the expression of p65 93 Table 1.
Biochanin A, isolated from Trifolium pratense L. Similarly, calycosin, formononetin, and ononin formononetinO-glucoside are reported to exhibit chondroprotective effects against inflammatory cytokines production, ECM degradation, and cell apoptosis by inhibiting the NF-κB signaling pathway in vivo and in vitro 95 , 96 , Table 1.
Aging, characterized by the accumulation of senescent cells and the resistance to apoptosis, is a risk factor for the development of various diseases and may increase the risk of hospitalization and death Aging has become the primary risk factor for OA development.
Chronic inflammation has been implicated in both OA development and the aging process. Potentially, targeting cellular aging has become a strategy to reverse the phenotype of OA chondrocytes Chondrocyte senescence can be regulated by IL-1β.
Silymarin has been shown to improve IL-1β-stimulated cell senescence, decrease catabolic gene expression, and restore chondrogenic phenotype factor expression The senescence-associated secretory phenotype SASP is associated with the biological actions of senescent cells in producing inflammation-promoting factors.
Similarly, Rhofolin exhibits significant effects against the expression of SASP factors and the phenotype of senescent cells by activating NRF2 signaling and suppressing the NF-κB pathway in IL-1β-treated chondrocytes Malvidin has been shown to relieve joint pain, downregulate the expression of the apoptotic marker β-galactosidase, and decrease the production of IL-1β, IL-6, TNFα, and MMPs by inactivating the NF-κB pathway in MIA-induced rat OA models 92 Table 1.
Balcalein has been reported to ameliorate oxidative stress , which has been known to contribute to cell senescence and chondrocyte apoptosis. However, post-treatment of chondrocytes with baicalein does not improve the expression of SASP factors, although it may restore mitochondrial viability and suppress chondrocyte apoptosis by inhibiting the NF-κB pathway Thus, the effects of natural flavonoids on OA chondrocyte senescence should be further elucidated.
The suppressive activity of natural flavonoids with different structures, such as the different positions and numbers of the hydroxyl group, has been comprehensively discussed recently However, these comparisons may be affected by different protocols and conditions.
Figure 4 The involvement of the NF-κB signaling in the pathological development of OA. The risk factors, such as age, trauma, inflammation, and obesity, can activate the NF-κB signaling, which up regulates the expression of IL-1β, IL-6, and TNFα.
The expression of catabolic enzymes, such as MMPs and ADAMTSs is enhanced by the NF-κB signaling, followed by ECM degradation and cartilage destruction.
The biological effects of flavonoids on inflammation might be affected by the number and position of substitutions. Hydroxyl groups in flavonoids may greatly contribute to their anti-inflammatory properties.
It has been shown that C-6 and C-7 hydroxyl group substitutions in flavones may promote anti-inflammation, and the hydroxyl group at the C-8 position suppresses the activity of anti-inflammation Quercetin flavonol has an OH group at the C-3 position, which is absent in luteolin flavone.
It has been reported that the IC 50 values of quercetin on LPS-stimulated NO This indicates that the OH group at the C-3 position displays a negative effect on anti-inflammatory activity. Furthermore, genistein an isoflavone has a higher IC 50 value Methoxylation of the OH group on a flavone often increases its anti-inflammatory activity.
For example, quercetin has a fold lower IC 50 value of 2. In TNFα-activated NF-κB signaling, 30 flavonoids were involved to explore the structure-activity relationship in suppressing NF-κB. A group with an electronegative property at C-5 of the A ring favors inactivating NF-κB through suppressing IKK activity.
Similarly, a bulky or hydrophobic substituent at the meta position of the B ring also contributes to NF-κB inactivation. However, substitutions in C-8 of the A ring decrease its activity Phosphorylation of IκBα contributes to the activation of NF-κB.
One study demonstrated that the hydroxyl groups in C-5, C-6, and C-7 can effectively increase the anti-inflammatory activity of flavones by suppressing IκBα phosphorylation, while almost all the other groups are insensitive to the inhibition of IκBα phosphorylation Flavonoids have been considered inhibitors of NF-κB signaling.
Similarly, quercetin, chrysin, pinocembrin, galangin, pinobanksin, and nobiletin can suppress NF-κB signaling by inhibiting IκBα and p65 phosphorylation and suppressing NF-κB nuclear translocation — However, cajanin but not prunetin can suppress the nuclear translocation of NF-κB Interestingly, apigenin, luteolin, and fisetin have been reported to inhibit the transcriptional activity of NF-κB but have not had any effects on IκBα degradation, p65 nuclear translocation, or pDNA binding In addition, acetylation may promote the transcriptional activity of NF-κB, and Sirt1 can induce the acetylation of NF-κB Fisetin has been reported to increase Sirt1 expression and decrease inflammatory responses in IL-1β-treated chondrocytes Flavonoids are the most abundant polyphenols with health-beneficial activity in plants and foods.
It is important for the food industry to supplement the aglycones, which have high absorption rates and plasma concentrations. Additionally, some therapeutic effects may be produced by the metabolites of these aglycones Natural flavonoids have been explored as a therapeutic strategy to manage bone diseases such as OA.
For example, Diosmetin exhibits protective activity against subchondral bone loss and cartilage degradation by decreasing the MAPK signaling pathway in RANKL-treated bone marrow-derived monocytes and DMM-induced mouse OA models The effectiveness of the flavonoids discussed above has been demonstrated.
However, the therapeutic efficacy in managing complex and chronic diseases, such as OA, by employing an individual candidate may be limited. Probably, a combination with other drugs may provide an effective approach.
Disappointingly, information about this strategy is rather limited. Although there are multiple beneficial pharmacological effects of flavonoids, studies on the therapeutic efficacy of flavonoids obtained from various resources in human beings are still needed.
It is crucial to note that flavonoids should be supplemented with caution, particularly those that may produce food—drug interactions and untoward reactions. In addition, useful strategies should be developed for increasing the efficiency of tissue-target delivery, enhancing bioavailability, and improving the therapeutic effects, although structural modifications of flavonoids have already been highlighted Recently, gut microbiota-regulated metabolism has been implicated in various fields.
Whether it poses an effect on the pharmacology of flavonoids still needs for further investigation. Great progress has been made in studying the pharmacological roles of natural flavonoids and their significance in the therapeutic management of OA. However, more exploration of the microbial metabolism of flavonoids is still needed due to their limited absorption characteristics and gut microbiome-regulated degradation in the colon.
Potentially, the microbial metabolites of flavonoids may be the effective compounds responsible for the pharmacological actions of the parent flavonoids.
The interaction between the gut microbiome and natural flavonoids should be included in the evaluation when exploring flavonoids to therapeutically manage OA. The underlying mechanisms of OA development are rather complicated, and they are the rational basis for new drug development.
Most clinical pharmacotherapies available for OA treatment are symptomatic. For instance, the role of IL-1β in the pathological development of OA has been demonstrated to be a target. An animal investigation using an IL-1 receptor antagonist has reported promising results. However, its biological effects on OA patients still need further investigation.
More efficient inflammatory biomarkers for predicting OA progression and treatment are needed to be further explored, and more potential drug targets are also needed to be discovered.
OA is characterized by low-grade chronic inflammation, and the inflammatory responses greatly promote the pathological changes and progression of OA.
Anti-inflammatory therapy has become an effective strategy for the therapeutic management of OA. The NF-κB signaling pathway plays a crucial role in inflammatory actions, which contribute to chondrocyte injury and ECM degradation.
Many inflammatory cytokines, such as IL-6 and TNFα, and ECM-degrading enzymes, such as MMPs and ADAMTSs, are transcriptional targets of the NF-κB pathway. Increased NF-κB pathway activity is associated with the pathological changes of OA, and targeting the NF-κB pathway has become an effective therapeutic strategy.
Flavonoids, the most abundant natural polyphenols, have been reported to have multiple pharmacological effects, particularly anti-inflammatory activity. A large body of research indicates that natural flavonoids protect against OA development by inactivating the NF-κB pathway, reducing the levels of inflammatory cytokines, and inhibiting the degradation of ECM Figure 5.
However, most studies focus on individual flavonoid compounds in protection against OA, which may have limited therapeutic efficacy. Additionally, clinical trials of natural flavonoids for humans are still rather rare. More efforts are still needed. Figure 5 Flavonoids protect against OA development by inhibiting the NF-κB-mediated inflammatory responses.
Activated NF-κB signaling increases the expression of IL-1β, TNFα, COX-2, PGE2, iNOS, NO, MMPs, and ADAMTSs, leading to the enhancement of ECM degradation, collagen II degradation, and chondrocyte apoptosis.
These catabolic responses can be blocked by flavonoids, such as myricetin My , quercetin Qu , morin Mo , baicalin Ba , luteolin Lu , chrysin Ch , EGCG EG , eriodictyol Er , and biochanin A Bi.
JZ: Conceptualization and methodology. JZ and YY: Data curation, writing-original draft preparation, data curation, validation, and writing-reviewing and editing. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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The complexity of human walking: a knee osteoarthritis study. PloS One 9 9 :e doi: CrossRef Full Text Google Scholar. Zhang W, Ouyang H, Dass CR, Xu J.
Current research on pharmacologic and regenerative therapies for osteoarthritis. Bone Res Jimi E, Fei H, Nakatomi C. NF-κB signaling regulates physiological and pathological chondrogenesis.
Int J Mol Sci 20 24 Li Z, Dai A, Yang M, Chen S, Deng Z, Li L. p38MAPK signaling pathway in osteoarthritis: Pathological and therapeutic aspects. J Inflammation Res — Shang X, Böker KO, Taheri S, Hawellek T, Lehmann W, Schilling AF. Int J Mol Sci 22 18 Thielen NGM, van der Kraan PM, van Caam APM.
Cells 8 9 Goldring MB, Marcu KB. Cartilage homeostasis in health and rheumatic diseases. Arthritis Res Ther 11 3 Min S, Wang C, Lu W, Xu Z, Shi D, Chen D, et al. Serum levels of the bone turnover markers dickkopf-1, osteoprotegerin, and TNF-α in knee osteoarthritis patients.
Clin Rheumatol 36 10 —8. Choi MC, Jo J, Park J, Kang HK, Park Y. NF-κB signaling pathways in osteoarthritic cartilage destruction. Cells 8 7 Chow YY, Chin KY. The role of inflammation in the pathogenesis of osteoarthritis. Mediators Inflammation Jiang N, Doseff AI, Grotewold E.
Flavones: From biosynthesis to health benefits. Plants Basel 5 2 Corcoran MP, McKay DL, Blumberg JB. Flavonoid basics: chemistry, sources, mechanisms of action, and safety. J Nutr Gerontol Geriatr 31 3 — Guo J, Ma J, Cai K, Chen H, Xie K, Xu B, et al. Isoflavones from semen sojae preparatum improve atherosclerosis and oxidative stress by modulating Nrf2 signaling pathway through estrogen-like effects.
Evid Based Complement Alternat Med Birt DF, Jeffery E. Adv Nutr 4 5 —7. Samadi F, Kahrizi MS, Heydari F, Arefnezhad R, Roghani-Shahraki H, Mokhtari Ardekani A, et al.
Quercetin and osteoarthritis: A mechanistic review on the present documents. Pharmacology — Chen X, Li Z, Hong H, Wang N, Chen J, Lu S, et al. Xanthohumol suppresses inflammation in chondrocytes and ameliorates osteoarthritis in mice.
BioMed Pharmacother Al-Khayri JM, Sahana GR, Nagella P, Joseph BV, Alessa FM, Al-Mssallem MQ. Flavonoids as potential anti-inflammatory molecules: A review.
Molecules 27 9 Oeckinghaus A, Ghosh S. The NF-kappaB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol 1 4 :a Hayden MS, Ghosh S.
Signaling to NF-kappaB. Genes Dev 18 18 — Shared principles in NF-kappaB signaling. Cell 3 — Britanova LV, Makeev VJ, Kuprash DV. Biochem Biophys Res Commun 3 —8. Kabe Y, Ando K, Hirao S, Yoshida M, Handa H. Redox regulation of NF-kappaB activation: distinct redox regulation between the cytoplasm and the nucleus.
Antioxid Redox Signal 7 — Li N, Karin M. Is NF-kappaB the sensor of oxidative stress? FASEB J 13 10 — Jin X, Song L, Liu X, Chen M, Li Z, Cheng L, et al. PloS One 9 12 :e Huang B, Yang XD, Lamb A, Chen LF. Posttranslational modifications of NF-kappaB: another layer of regulation for NF-kappaB signaling pathway.
Cell Signal 22 9 — Zhou Y, Jin X, Yu H, Qin G, Pan P, Zhao J, et al. HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer. Theranostics 12 5 — Chen LF, Williams SA, Mu Y, Nakano H, Duerr JM, Buckbinder L, et al. NF-kappaB RelA phosphorylation regulates RelA acetylation.
Mol Cell Biol 25 18 — Goldenberg DL, Egan MS, Cohen AS. Inflammatory synovitis in degenerative joint disease. J Rheumatol 9 2 —9. Google Scholar. Liu-Bryan R, Terkeltaub R. Emerging regulators of the inflammatory process in osteoarthritis. Nat Rev Rheumatol 11 1 — Zahan OM, Serban O, Gherman C, Fodor D.
The evaluation of oxidative stress in osteoarthritis. Med Pharm Rep 93 1 — Kulkarni P, Martson A, Vidya R, Chitnavis S, Harsulkar A. Pathophysiological landscape of osteoarthritis.
Adv Clin Chem — Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev 1 :8— Roškar S, Hafner-Bratkovič I.
The role of inflammasomes in osteoarthritis and secondary joint degeneration diseases. Life Basel 12 5 Li Y, Mai Y, Cao P, Wen X, Fan T, Wang X, et al. Relative efficacy and safety of anti-inflammatory biologic agents for osteoarthritis: A conventional and network meta-analysis.
J Clin Med 11 14 De Luca F. Role of nuclear factor kappa b NF-κB in growth plate chondrogenesis. Pediatr Endocrinol Rev 13 4 — Kanegae Y, Tavares AT, Izpisúa Belmonte JC, Verma IM.
Nature —4. Wu S, Morrison A, Sun H, De Luca F. Nuclear factor-kappaB NF-kappaB p65 interacts with Stat5b in growth plate chondrocytes and mediates the effects of growth hormone on chondrogenesis and on the expression of insulin-like growth factor-1 and bone morphogenetic protein J Biol Chem 28 — Caron MM, Emans PJ, Surtel DA, Cremers A, Voncken JW, Welting TJ, et al.
PloS One 7 3 :e Olivotto E, Borzi RM, Vitellozzi R, Pagani S, Facchini A, Battistelli M, et al. Differential requirements for IKKalpha and IKKbeta in the differentiation of primary human osteoarthritic chondrocytes. Arthritis Rheum 58 1 — Saito T, Tanaka S.
Molecular mechanisms underlying osteoarthritis development: Notch and NF-κB. Arthritis Res Ther 19 1 Hirata M, Kugimiya F, Fukai A, Saito T, Yano F, Ikeda T, et al. Hum Mol Genet 21 5 — de Andrés MC, Imagawa K, Hashimoto K, Gonzalez A, Roach HI, Goldring MB, et al.
Loss of methylation in CpG sites in the NF-κB enhancer elements of inducible nitric oxide synthase is responsible for gene induction in human articular chondrocytes. Arthritis Rheum 65 3 — Latourte A, Cherifi C, Maillet J, Ea HK, Bouaziz W, Funck-Brentano T, et al.
Ann Rheum Dis 76 4 — Nakatomi C, Nakatomi M, Matsubara T, Komori T, Doi-Inoue T, Ishimaru N, et al. Constitutive activation of the alternative NF-κB pathway disturbs endochondral ossification. Bone — Soysa NS, Alles N, Weih D, Lovas A, Mian AH, Shimokawa H, et al.
The pivotal role of the alternative NF-kappaB pathway in maintenance of basal bone homeostasis and osteoclastogenesis. J Bone Miner Res 25 4 — Ishikawa H, Carrasco D, Claudio E, Ryseck RP, Bravo R. Isoflavones also reduced IL-8 via TNF-α inhibition in Caco-2 cell lines.
Genistein is also known to mimic oestrogen and reduce IBD symptoms. Moreover, genistein inhibited MPO and COX2 activity via the NF-κB pathway. Daidzein is one of the isoflavones that reduces IL6-, IL-8, IL, INF-γ, and up-regulates IL in mesenteric lymph node cells in DSS-induced colitis [ 40 ].
Naringin decreased xanthine oxidase, alkaline phosphatase, MPO, malondialdehyde MDA , and NO. They also downregulated iNOS, ICAM-1, MCP-1, IL-6, MIP-2, PGE 2 , INF-γ, and ILA. This reduced DSS-induced colitis. Hesperidin also reduced colitis by attenuating MDA, MPO, and IL Anthocyanins also show anti-inflammatory properties and reduce pro-inflammatory cytokines.
Anthocyanins reduce IBD by minimising the expression of IL-6, IL-9, INF-γ, MPO, TNF-α, IL-1β, ILA, iNOS, and COX2. Apigenin and luteolin decreased IBD by regulating TNF-α, IL-1β, iNOS, and COX2 expression.
Diosmin acted on LTB4 MPO to increase GSH levels. Wogonin and tangeretin increased claudin-1 zonula occluden-1 in the tight junctions.
They also reduced IL-6, IL-1β, IL-8, iNOS, and COX2; and TLR4, MyD88, TGF-β-activated kinase 1 TAK1 , IL, and TNF-α expression. Tangeritin also decreased T helper cells in Th1 and Th17 differentiation [ 40 ].
Effect of Flavonoids in Cancer Treatment Inflammation is responsible for controlling many cellular pathways, for which its unregulated expression leads to cancer. Hence, inflammation is a hallmark of cancer initiation and progression. The anti-inflammatory property of flavonoids also reduces cancer progression; hence, flavonoids show anti-cancer activities as well.
Hesperidin was seen to decrease cell viability in the C6 glioma cell line [ 41 ]. Flavonoids also inhibit fibroblast differentiation into cancer-associated fibroblast by targeting TGF-β2 [ 42 ].
In a study by Hou et al. Flavonoids are studied to decrease C-X-C motif chemokine receptor 4 CXCR4 expression, which reduces metastasis. Ageratum conyzoides L. showed a cytotoxic effect against mouse leukaemia cells and human non-small lung cancer cells [ 44 ].
It also inhibited the growth of glioblastoma cell lines and prostate cancer cell lines [ 45 ] [ 46 ]. Flavonoids in A. conyzoides inhibit the proliferation of HeLa cells by inducing S phase arrest in the cell cycle. They also induced apoptosis in HeLa cells [ 45 ].
Flavonoids from Chinese bayberry induced G1 phase arrest in ovarian cancer cells [ 48 ]. The flavonoids of Citrus platymamma Hort. Further reports suggest that luteolin and quercetin could attenuate EMT, thereby reducing the progression of cancer in squamous carcinoma cells [ 52 ].
Isoliquiritigenin, a flavonoid from licorice, inhibited EMT in ovarian cancer cells [ 53 ]. In a study, cells treated with flavonoid from A. Conyzoides showed enhanced E-cadherins and reduced N-cadherins and vimentin in xenograft tumours, thereby inhibiting invasion and migration of HeLa cells [ 45 ].
References Serafini, M. Flavonoids as Anti-Inflammatory Agents. Ferraz, C. Therapeutic Potential of Flavonoids in Pain and Inflammation: Mechanisms of Action, Pre-Clinical and Clinical Data, and Pharmaceutical Development.
Molecules , 25, Cunha, T. USA , , — Sachs, D. Gao, W. Quercetin ameliorates paclitaxel-induced neuropathic pain by stabilizing mast cells, and subsequently blocking PKCε-dependent activation of TRPV1. Acta Pharmacol. Farzaei, M. Targeting Inflammation by Flavonoids: Novel Therapeutic Strategy for Metabolic Disorders.
Carvalho, T. The Granulopoietic Cytokine Granulocyte Colony-Stimulating Factor G-CSF Induces Pain: An-algesia by Rutin. Inflammopharmacology , 27, — Iio, M. Effects of Baicalein, a Flavonoid, and Other Anti-inflammatory Agents on Glyoxalase-I Activity.
García-Lafuente, A. Flavonoids as Anti-Inflammatory Agents: Implications in Cancer and Cardiovascular Disease. Liskova, A. Flavonoids against the SARS-CoV-2 induced inflammatory storm. Ruiz-Iglesias, P.
Influence of Hesperidin on Systemic Immunity of Rats Following an Intensive Training and Exhausting Exercise. Nutrients , 12, Choy, K. Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B NFκB Signaling in Cardiovascular Diseases: A Mini Review. Kang, O. Luteolin isolated from the flowers of Lonicera japonica suppresses inflammatory mediator release by blocking NF-κB and MAPKs activation pathways in HMC-1 cells.
Molecules , 15, — Lee, K. Andrographolide acts as an anti-inflammatory agent in LPS-stimulated RAW Zhang, J. Systems Pharmacology Dissection of the Anti-Inflammatory Mechanism for the Medicinal Herb Folium Eriobotryae. Hämäläinen, M.
Anti-inflammatory effects of flavonoids: Genistein, kaempferol, quercetin, and daidzein inhibit STAT-1 and NF-κB activations, whereas flavone, isorhamnetin, naringenin, and pelargonidin inhibit only NF-κB activation along with their inhibitory effect on iNOS expression and NO production in activated macrophages.
Jiang, J. Vitexin suppresses RANKL-induced osteoclastogenesis and prevents lipopolysaccharide LPS -induced osteolysis. Borghi, S. Vitexin inhibits inflammatory pain in mice by targeting TRPV1, oxidative stress, and cytokines.
Ye, M. Cell Biol. Chen, X. Heart Circ. Phys Iol. Imam, F. Rutin attenuates carfilzomib-induced cardiotoxicity through inhibition of NF-κB, hypertrophic gene expression and oxidative stress. Li, X. Effect of chrysin on expression of NOX4 and NF-κB in right ventricle of monocrotaline-induced pulmonary arterial hypertension of rats.
Yao Xue Xue Bao Acta Pharm. Yang, M. Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction. Al-Ishaq, R. Flavonoids and their anti-diabetic effects: Cellular mechanisms and effects to improve blood sugar levels.
Biomolecules , 9, Bule, M. Antidiabetic effect of quercetin: A systematic review and meta-analysis of animal studies. Food Chem. Ola, M. Neuroprotective Effects of Rutin in Streptozotocin-Induced Diabetic Rat Retina.
Wang, Y. Therapeutic potential of Oroxylin A in rheumatoid arthritis. Lee, J. Anti-inflammatory effects of oroxylin A on RAW Yang, J. Identification of Baicalin as an Immunoregulatory Compound by Controlling TH17 Cell Differentiation.
PLoS ONE , 6, e Yang, X. Baicalin Inhibits ILMediated Joint Inflammation in Murine Adjuvant-Induced Arthritis. Kelepouri, D.
Chronic inflammation arthrktis being shown to be increasingly involved in the onset and development Fuel Usage Optimization several pathological disturbances Enhance metabolic activity as arteriosclerosis, obesity, diabetes, neurodegenerative diseases and Flavonnoids cancer. Treatment for chronic inflammatory disorders has not been agthritis, and there is arthritie urgent Fuel Usage Optimization to find new and safe anti-inflammatory compounds. Flavonoids belong to a group of natural substances occurring normally in the diet that exhibit a variety of beneficial effects on health. The anti-inflammatory properties of flavonoids have been studied recently, in order to establish and characterize their potential utility as therapeutic agents in the treatment of inflammatory diseases. Several mechanisms of action have been proposed to explain in vivo flavonoid anti-inflammatory actions, such as antioxidant activity, inhibition of eicosanoid generating enzymes or the modulation of the production of proinflammatory molecules.
Agthritis, Myrtaceae. Zrthritis structures of atthritis compounds were elucidated artritis spectroscopic means. The cytotoxicity of the compounds was evaluated against the RAW arthritix The arthrtis and artjritis activities were evaluated afthritis measuring inflammatory parameters in lFavonoids models.
The Arthritie glycosylated Flavonoids and arthritis inhibited the Multivitamin for heart health of tumor necrosis factor-α in RAW Roberto Mikio Kassuya, Elisangela Flavoniids Santos, … Flavlnoids Gasparotto Junior.
Yongliang Tang, Daotao Arthriyis, … Yi Qiang. Sonia Amador, Antonio Nieto-Camacho, … Emma Muscular endurance for athletes. Inflammation is a Falvonoids of self-protection Flavonoisd the Flavonoida against the harmful agents that are involved in damaging the cells, tissues, and organs Kuprash and Nedospasov Inflammation is providing assistance to the arthritjs to get rid abd harmful agents, and Replenish Physical Energy tissue components, so that the body can begin to heal Kuprash and Nedospasov During an Flavvonoids reaction swelling, loss of function anf pain are the dominating signs of Sports nutrition and carbohydrate intake because of the release of various inflammatory cytokines such as tumor necrosis factor-α TNF-α Zelová and Fuel Usage Optimization Healthy weight loss habits However, prolonged existence of arthrtis inflammation gives rise to the Flavonoidz of Flvonoids diseases such as Replenish Physical Energy arthritis RA Harth and Nielson Indeed, TNF-α is known to be arthitis potent inducer of other pro-inflammatory Electrolytes and pH balance including interleukin Flavonlids IL-1βchemokines, and proteases Farzaei et al.
Conventionally, the treatment of RA is based upon disease-modifying arhhritis drugs arthritix methotrexate, Flaavonoids slow down joint damage Healthy weight management articles reduce joint swelling arthritiis pain Friedman and Cronstein However, treatment of Arthrjtis has been revolutionized by the discovery artbritis the role of certain cytokines, in particular TNF-α, Flavonoids and arthritis arthriits pathogenesis of the disease Arthtitis et al.
Since the first arthirtis of TNF-α inhibitors in RA in the s, drugs as adalimumab, certolizumab arthriis, etanercept, Flavonoidx, and infliximab Flavonoidds shown improving arthgitis, functional, and Type diabetes blood sugar spikes outcomes in patients arthrits RA disease Abbasi et Flavonods.
Therefore, it has become zrthritis and essential to develop safer and more cost-effective TNF-α inhibitors. In nature, many arthitis compounds belonging Replenish Physical Energy various classes have been found Fllavonoids reduce TNF-α levels Ye et al. These Flavonoid compounds have been found to interfere Flqvonoids various pro-inflammatory mediators, such as nuclear factor kappa-light-chain-enhancer of activated B cells NF-κB abd other signaling molecules, qrthritis in TNF-α expression Flavnoids, thus, they could Essential vitamins chart an Circadian rhythm hormone secretion means atrhritis treating RA, modulating the production, rather than the activity of TNF-α Doss et nad.
The genus Syzygium is one of genera about species belonging to the family Myrtaceae which arthritls native to the tropics, particularly, in tropical America and Arthritiss de Paulo Farias et al. Many species of this genus are used arthritiss to treat digestive tract disorders, dental pain, and arthritis Chua et al.
Syzygium jambos L. The Optimal athletic nutrition of the fruit and leaves are athritis used for its antipyretic Fuel Usage Optimization anti-inflammatory properties, such as gastrointestinal disorders, rheumatism, and tooth ailments and to relieve sore eye conditions Chua et Flaonoids.
The pharmacological value of S. jambos has been documented Haque et al. Generally, arthritiss aqueous and alcoholic Flavonoisd have Flavoboids a promising anti-inflammatory activity Hossain et al. Flavonoixs investigation of Natural hair care products active extracts arthrtiis several secondary metabolites.
For instance, flavonoids, tannins, and triterpenoids Sobeh et Flavoniods. Slowing Enhancing performance while managing dietary limitations al.
Accordingly, the aand work was carried out to evaluate Flvonoids anti-inflammatory and arthriis activities of the aqueous extract of S. Flavonoide and Flavonoivs of its isolated glycosylated flavonoids 1 Flaconoids 2 in the edematogenic agent-induced mice paw Flavonoide.
Thin-layer Herbal remedies for muscle recovery was performed using Merck Herbal dietary supplements gel Herbal extract blends plates, which were anf by UV absorbance arthrihis.
Developed plates were stained with phosphomolybdic acid H 3 PMo 12 O 40 solution in ethanol for detection through heating. Open column chromatography was performed with silica gel 20—45 and 40—63 μm. Nuclear magnetic resonance NMR experiments were performed on a Bruker Analytische Messtechnik GmbH spectrometer operating at MHz 1 H or 75 MHz 13 C and Bruker BioSpin GmbH operating at MHz 1 H or 76 MHz 13 C.
Spectra were calibrated by assignment of the residual solvent peak to δ H 7. The leaves of Syzygium jambos L. The botanical identification was confirmed by Dr.
Antonio Galán, the Botany Department Herbarium of the Faculty of Pharmacy Universidad Complutensewhere a sample was deposited herbarium number The air-dried leaves g were extracted by decoction 30 min at boiling point with distilled water g.
The resulting aqueous extract was frozen in glass containers at a temperature of — 38 °C and then lyophilized Freeze dryer, Christ alpha 1e2 LD plus, Germany at — 50 °C.
Each fraction was evaluated for its cytotoxicity and anti-inflammatory activities. Fractions VIII 3. The chromatographic profile analysis of these fractions showed that they were similar, so they were pooled. Five sub-fractions 1—5 were obtained and all of them showed anti-inflammatory activity, but sub-fractions 4 1 g and 5 0.
The 1 H and 13 C NMR spectroscopic data were identical with those previously described Slowing et al. For this assay, the protocol developed by Apaza Ticona et al.
RAW After h incubation, the old medium was removed and the cells were filled with μl of fresh medium treated with the samples to be analyzed.
Subsequently, from the stock solutions, a series of dilutions were performed until a final DMSO concentration of 0. After the treatment with the samples, μl of culture medium supernatants was collected and incubated in the reaction mixture of the LDH kit.
After 30 min, the reaction was stopped by the addition of 1 N HCl, and the absorbance at a wavelength of nm was measured using a spectrophotometric ELISA enzyme-linked immunosorbent assay plate reader, SpectraMax® i3, Molecular Devices, CA, USA.
The protocol developed by Tena Pérez et al. The cells were then treated with the extracts, fractions, and compounds at the same concentrations used in the viability assays for 2 h, before stimulation with 0.
Absorbance was read at nm on a spectrophotometric ELISA plate reader Anthosversion 2. The anti-inflammatory activity of the aqueous extract, fractions, and isolated compounds was evaluated by the method of carrageenan-induced inflammation in the anterior paw of the mice as described by Apaza Ticona et al.
Seven groups 5 mice for group were selected for this study. was selected for the treatments of extracts, fractions, and compounds based on the protocol of Apaza Ticona et al. After 30 min of the intraperitoneal treatment of the animals of groups 3—7 with IND and the samples extract, fractions, and compoundsthe inflammation was induced by the injection of 50 μl of CARR solution type IV Sigma Chemical Company, USA into the right hind paw of each mouse.
The thickness of the paw edema was measured immediately after CARR injection and during the 6 h following the induction of the edema at an interval of 1 h after the administration of the edematogenic agent using a plethysmometer modelIITC Life Science, Woodland Hills, CA.
All the assessments were performed by the same investigator in order to reduce any potential inter-operator differences. The size of the edema was calculated as follows:.
The anti-inflammatory activity was calculated as a percentage of inhibition of edema by the extract in treated animals under test in comparison with the CARR control group.
The animals were sacrificed after 6 h. The CARR-induced edema feet were dissected and stored at — 70 °C. Blood samples were taken from anesthetized mice 6 h after the CARR administration and kept at — 70 °C.
According to the type of assay, samples were taken: in citrate tubes to be centrifuged for 15 min at relative centrifugal force RCF obtaining a plasma isolate to analyze TNF-α, in heparin tubes to be centrifuged for 15 min at RFC obtaining a plasma isolate to analyze C-reactive protein CRPand in citrate tubes to be centrifuged for 15 min at RFC obtaining a plasma isolate to analyze fibrinogen.
TNF-α was determined from a standard curve. The CRP dosage was determined by an automatic analyzer COBAS INTEGRA plus analyzer C-reactive.
The results were automatically calculated in terms of concentration. The CRP level is expressed in milligrams per liter of serum. The plasma fibrinogen assay was determined according the methodology described by Apaza Ticona et al.
Then, the reagent STA-Fibrinogen was added. The level of fibrinogens in the tested samples is expressed in grams per liter of plasma. Experimental arthritis was induced in mice according to the method used by Apaza Ticona et al. Eight groups five mice for group were selected for this study.
The edema and inflammatory parameters were measured with the same methods described above. All the experiments were performed in triplicate. All the analyses were performed using GraphPad Prism, version 9. Software CA, USA. The objective of the present investigation was to provide preliminary evidences for the ethnopharmacological use of this species as an antipyretic and anti-inflammatory cure rheumatism Chua et al.
First, the viability of the RAW Previously, Rocchetti et al. jambosshowing no high cytotoxicity, due to the chemical composition of the extract, being mainly phenolic compounds. These results show that both fractions have anti-inflammatory activity by inhibiting the cytokine TNF-α, which is one of the main pro-inflammatory cytokines involved in the pathogenesis of chronic inflammatory diseases.
It also triggers the cellular release of other cytokines, chemokines, or inflammatory mediators Zelová and Hošek The analysis of the inhibitory activity of TNF-α obtained with the different treatments indicated that the differences in the IC 50 values are due to their chemical composition.
For the aqueous fraction, and according to its proton spectrum Fig. In the case of n -C 7 H 16 fraction, the presence of fatty acids 2. Finally, in the proton spectrum of the aqueous fraction Fig. From these results, it can be concluded that the presence of polyphenolic compounds is relevant for the anti-inflammatory activity.
As shown in Fig. The edema size variation follows a polynomial function. In fact, 2 h after CARR injection, the size of the edema reached a maximum which indicates an acute inflammation; this effect of increasing edema increase in inflammatory mediators after 2 h of CARR injection has already been reported by other researchers Makni et al.
Edema size evolution over time in the different groups of mice treated with the aqueous extract Aq. E and fractions HEP. Control untreated control mice. Each value represents the mean ± SEM of results from six animals. Regarding the anti-arthritic activity, the sub-plantar injection of CFA led the paw to swell gradually for more than 14 days.
: Flavonoids and arthritis| Flavonoids: Broad Spectrum Agents on Chronic Inflammation | Kim, CS, Choi, HS, Joe, Y, Chung, HT, and Yu, R a. Kaempferol inhibits the migration and invasion of rheumatoid arthritis fibroblast-like synoviocytes by blocking activation of the MAPK pathway.. Zhang, J. It was also observed in a study that procyanidin in apples could reduce IFN-γ and IL [ 31 ]. Life Sci. |
| The therapeutic potential of plant flavonoids on rheumatoid arthritis | Flavonouds GJ, Goodridge HS, Harnett MM, Wei SQ, Nikolaev AV, Higson AP, et al. Article Google Scholar Luo C, Xu X, Wei X, Feng W, Huang H, Liu H, et al. Peng, L. Seo, S. Am J Chin Med. |
| Top bar navigation | Thus, whether flavonoids targeting inflammasome components in canonical pathway can also affect these components involved in noncanonical inflammasome pathways should be further studied. Wang, Z, Ka, SO, Lee, Y, Park, BH, and Bae, EJ b. Anti-infective properties of epigallocatechingallate EGCG , a component of green tea. Chemokines in the pathogenesis of vascular disease. Icariin, a prenylated flavonoid, blocks the STAT3 pathway, hence reducing IL and Th17, which reduces the cartilage and bone degradation in CIA mice [ 32 ]. Harth M, Nielson WR Pain and affective distress in arthritis: relationship to immunity and inflammation. Article Google Scholar Lee CJ, Moon SJ, Jeong JH, Lee S, Lee MH, Yoo SM, et al. |
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