EGCG and inflammation-related diseases -
In addition, in vivo angiogenesis and granulation tissue augmentation by GTE have been demonstrated [ 30 ]. Therefore, further animal model research is needed. In summary, our results sustained the hypothesis that GTE attenuates the inflammation in gingival epithelial keratinocytes treated with LPS by downregulating inflammatory cytokines in a dose-dependent manner.
The results from our experiment support that GTE can be considered a potent anti-inflammatory agent with a potential as an oral therapeutic against inflammation.
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Int J Morphol — Download references. FIGURE 4. Effect of EGCG on airway mucus secretion in rats. A Representative photomicrographs of lung sections stained with periodic acid Schiff PAS. Goblet cells appear as purple staining arrows over epithelium. PAS staining revealed increased goblet cell metaplasia after CS exposure and EGCG reduced the CS-induced goblet cell metaplasia.
MUC5AC-positive staining showed similar phenomenon of mucus secretion of PAS-staining in different groups. Scale bar, μm. C Quantification of PAS-positive cells per length of epithelium for goblet cells of different groups. D Quantification of MUC5AC-positive cells per length of epithelium for mucin of different groups.
MUC5AC is recognized as the major secreted airway mucins, which is highly expressed in the goblet cells of the airway epithelium. Immunohistochemical experiment showed that the MUC5AC-positive cells were co-localized in PAS-stained goblet cells Figure 4B. Therefore, EGCG could inhibit CS-induced mucus hypersecretion in the airways of rats.
Small airway remodeling is a common feature of COPD patients. The sub-epithelial deposition of collagen in airways of medium size indicates fibrosis. FIGURE 5. Effect of EGCG on airway fibrosis in rats. Rats treated with EGCG or control vehicle were killed on day 57 and the left lung was formalin-fixed and sectioned for histology magnification × To further explore the mechanism how EGCG ameliorated CS-induced mucus hypersecretion, the changes of protein expression of p-EGFR and EGFR were detected using Western blot analysis.
CS exposure upregulated the expressions of p-EGFR and EGFR by 4. FIGURE 6. Effect of EGCG on the activation of EGFR in rats. A Representative photographs of Western blot for p-EGFR and EGFR proteins from homogenized rat lung tissue were shown. EGFR, epidermal growth factor receptor.
In this study, we demonstrated that the imbalance of serum levels of oxidants and antioxidants by CS exposure was reversed by EGCG administration, in support of EGCG being an antioxidant. We further found that EGCG inhibited CS-induced goblet cell hyperplasia and reduced number of MUC5AC-positive cells in the airways, CINC-1 production, neutrophil infiltration and collagen deposition probably via the inhibition of EGFR activation in rat lung.
To the best of our knowledge, this is the first study to reveal the signaling pathway involved in EGCG-mediated inhibition of mucus hypersecretion in vivo.
In contrast to our previous study, Chinese green tea Lung Chen caused body weight loss Chan et al. At baseline, the body weight was similar among all groups. By week 8, the weight gain in the CS group was slightly lower than in the SA group data not shown. Therefore, the loss of body weight from green tea should be due to the presence of the combination of catechins rather than EGCG alone.
In the current study, serum 8-isoprostane, a biomarker of oxidative stress, was increased after CS exposure in agreement with COPD patients and animal studies Chan et al.
Another oxidative stress biomarker AOPP, as a measure of protein oxidation caused by the chlorinated oxidants, was associated with the status of smoking in humans Vargas et al. In response to the increase in oxidant load, we found a decrease in serum T-AOC, and a reduction in activities of both SOD and catalase upon CS exposure.
In agreement, T-AOC in saliva was reduced in smokers compared with non-smokers Bakhtiari et al. GSTs, phase II enzymes that catalyze the conjugation of electrophilic molecules with glutathione GSH to detoxified conjugates were increased in mild COPD patients but reduced in severe COPD patients Harju et al.
In this study, we found an increase in serum GST levels after CS exposure, indicating that our animal model mimics milder stages of human COPD. Smoking is regarded as one of major risk factors in chronic inflammatory lung diseases. Components of CS have strong oxidative effects and are believed to drive the downstream inflammatory processes, especially in the small airways Hogg, Our previous study also demonstrated that CS caused infiltrations of macrophages and neutrophils in the airways Li et al.
In this study, we focused on CINC-1 resemble to human IL-8 and MCP-1, which regulate the recruitment and maturation of neutrophils and macrophages, respectively. Higher gene expression levels of IL-8 and MCP-1 were found in the bronchiolar epithelium of subjects with COPD de Boer et al. Upon CS exposure, both CINC-1 and MCP-1 were upregulated in serum and BALF.
Interestingly, EGCG administration reduced the levels of CINC-1 in both serum and BALF, but not MCP-1 in BALF Figure 2 , suggesting the presence of differential effects. The exact mechanism in which EGCG mediates such an effect may be due to direct binding to the chemokines and limiting their biological activities Qin et al.
The mechanism for the differential effects between serum and BALF MCP-1 was currently unclear. In this study, EGCG was administered via oral gavage with its active ingredients absorbed into the blood stream. Neutrophils are recruited into the lung from the circulation via CINC-1 as chemoattractant.
On the other hand, there are two types of macrophages found in the lung, i. MCP-1 plays a critical role in regulating the activation and recruitment of cells of the monocytic lineage.
Therefore, the predominant resident alveolar macrophages may not be an essential target of EGCG via oral gavage to detect an inhibitory effect on MCP-1 in BALF.
Although there was no inhibition of CS-induced elevation of MCP-1 in BALF, EGCG significantly inhibited CS-mediated recruitment of neutrophils, in line with the inhibition of CINC-1 in both serum and BALF. Mucus is essential because of its role in protecting the airways.
However, chronic inflammatory lung diseases, such as COPD, are often associated with excessive mucus production, especially in cases of chronic bronchitis. Cigarette smoke is a common stimulus that promotes mucus secretion and has a great effect on promoting the synthesis and secretion of MUC5AC mucin Haswell et al.
MUC5AC has been recognized as the predominant mucin in human airway epithelial cells, and its expression increases in smokers and patients with COPD Di et al.
In this study, CS exposure caused increased numbers of goblet cells and the MUC5AC-positive cells in the airways of rats as an indicator for the production of more mucus due to oxidative stress.
In agreement, oxidants were found to be involved in mucus hypersecretion and impairment of mucociliary clearance Fischer et al. Hydrogen peroxide and superoxide were shown to cause increased mucus secretion in airway epithelial cells Adler et al.
Our data revealed that EGCG reversed the activities of SOD and CAT, which could reduce the levels of hydrogen peroxide and superoxide, resulting in attenuation of mucus production, which may suggest the partial attribution of antioxidative effect of EGCG on mucus secretion.
Neutrophils are the predominant inflammatory cells in the airways of patients with COPD. Neutrophilic products, such as proteases and oxidants, have been evaluated for their roles in regulating mucin gene expression. NE, a serine protease, is regarded as a major product from activated neutrophils to be implicated in airway inflammation, goblet cell metaplasia, structural lung damage, and host defense Gehrig et al.
NE, which can then act directly on the epithelium Takeyama et al. In the present study, the neutrophil counts were elevated in CS-exposed rats and significantly lowered in EGCG-pretreated rats. Therefore, the inhibitory effect of EGCG on mucus hypersecretion may be partly due to the inhibition of neutrophil infiltration.
The EGFR signaling pathway is a receptor tyrosine kinase and plays a regulatory role in airway mucus production and secretion Ha and Rogers, Takeyama et al. Furthermore, Takeyama demonstrated that CS exposure upregulated EGFR mRNA expression and induced EGFR-specific tyrosine phosphorylation, resulting in increased MUC5AC mRNA and protein production, such effects that were inhibited completely by selective EGFR tyrosine kinase inhibitors Takeyama et al.
In this study, CS increased the neutrophil infiltration in the airways, increased p-EGFR and EGFR protein levels in rat lung tissue, resulting in increased MUC5AC production, which was inhibited in the presence of EGCG, indicating the protective effect on CS-mediated airway mucus hypersecretory diseases through the EGFR pathway.
In support of our findings, the theaflavins isolated from black tea and ECG extracted from green tea have been reported to inhibit mucin secretion possible via EGFR pathway Kim et al. Pulmonary fibrosis is a hallmark of repeated cycles of dysregulated repair and remodeling of the lung parenchyma, causing decreased airway elasticity.
The role of fibrosis in COPD is somewhat controversial but recent evidence suggests that fibrosis and COPD do co-exist, usually in smokers Jankowich and Rounds, Collagen fibers, being one of the main components of the extracellular matrix, undergo constant remodeling upon injury caused by exposure to CS McKleroy et al.
Increased collagen deposition was found to correlate with lung destruction in human emphysema Martin-Mosquero et al. In this study, rats exposed to CS increased collagen deposition in the lung, which was attenuated by EGCG treatment. The exact mechanisms involved are not entirely clear, although some studies have inferred that catechins are potentiating stabilization of collagen fibers as well as the inhibition of collagenases Madhan et al.
Our data demonstrate that EGCG has a protective effect on CS-induced oxidative stress, airway neutrophilic inflammation, and airway mucus production in rat lungs probably via inhibition of EGFR signaling pathway, leading to amelioration of airway remodeling Figure 7.
EGCG may be a promising therapeutic strategy to limit neutrophil recruitment and to treat mucus hypersecretion in the airways of smokers without or with COPD. FIGURE 7. Schematic diagram. Cigarette smoke CS exposure causes oxidative stress, inflammation, and airway mucus production.
This article does not contain any studies with human participants performed by any of the authors. All procedures performed in studies involving animals were in accordance with the ethical standards of the Committee on the Use of Live Animal in Teaching and Research CULATR in the University of Hong Kong with the approval number YL conceived, performed and interpreted the experiments and wrote the draft of the manuscript.
KL helped with experimental design and writing the draft of the manuscript. SY helped with the animal study and section staining, and analyzed the data. XL helped with the animal study and sample preparation.
MI helped with the experimental design and editing the manuscript. JM conceived, interpreted the experiments and assisted with editing the manuscript.
All authors reviewed and approved the manuscript. This work was supported by National Natural Science Fund of China NSFC; No. 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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Background: Cigarette smoking is Blood pressure monitoring tools leading cause of chronic Nutritious foods for injury recovery pulmonary disease. Diseasez this study, we inflaammation-related to analyze the effects of EGCG on intlammation-related Nutritious foods for injury recovery CS -induced airway inflammation and mucus secretion in the CS-exposed rat model. Methods: Male Sprague-Dawley rats were randomly divided into either sham air SA or CS exposure. was given by oral gavage every other day in both SA and CS-exposed animals. Western blot analysis was performed to explore the effects of EGCG on epidermal growth factor receptor EGFR -mediated signaling pathway. Inflammztion-related Green Healthy respiratory system has been shown to have beneficial effects against a variety Nutritious foods for injury recovery diseases such as inflammatio-nrelated, obesity, diabetes, cardiovascular disease, and disease diseases. Through cellular, animal, and human Recharge with No Hidden Charges, green Immune system-boosting herbs and its major component, epigallocatechingallate EGCG have been demonstrated to have anti-inflammatory effects. We also reviewed results from cellular and animal experiments and proposed action mechanisms. Results: Most of the results from the human studies indicated the beneficial effects of green tea and tea catechins against inflammatory diseases. Conclusion: Since green tea and EGCG have multiple targets and act in a pleiotropic manner, we may consider their usage to improve the quality of life in patients with inflammatory disease.
Es ist einfach unvergleichlich:)
Ja ist es aller die Phantastik