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5 Natural Pain Killers That Actually Work!Flavonoids as natural pain relievers -
Conversely, selective sodium Na channel blockers such as lidocaine and carbamazepine inhibit the generation of ectopic impulses that reduces the sensation of neuropathic pain. On the other hand, the hyperexcitability of the central dorsal horn is caused by spinal cord injury that subsequently decreases intraspinal inhibitory interneurons, which finally leads to neuropathic pain.
However, GABA agonists, including baclofen, inhibit the decreased intraspinal inhibitory interneurons that plays an essential role in reducing the sensation of neuropathic pain.
DRG, dorsal root ganglion; Na, sodium. Overexpression of messenger ribonucleic acid mRNA for voltage-gated sodium channels in the primary afferent neurons is accountable for ectopic spontaneous activity after nerve damage.
This event might cause the clustering of these channels, which declines the action potential threshold, leading to hypersensitivity. Therefore, sodium channel blockers, including lidocaine, demonstrate pain relief action in NP through this mechanism Lai et al.
Peripheral nerve injury is also responsible for the upregulation of various receptor proteins. These receptors are usually found at the membranes of the primary afferents and are partly expressed during physiological conditions. Vanilloid receptors, including the transient receptor potential cation channel subfamily V member 1 TrpV1 , play a crucial role in the sensing of toxic heat exceeding 43°C Patapoutian et al.
Furthermore, the TRPM8 receptor is expressed in neurons that are small in diameter from the dorsal root ganglia McKemy et al.
Nerve injuries can cause the upregulation of this channel, contributing to peripheral sensitization of C-nociceptors, which results in cold hyperalgesia Wasner, In addition, acid-sensing ion channels are thought to take part in static mechanical hyperalgesia Price et al.
In contrast, both α 1 - and α 2 -adrenoceptors situated on the cutaneous afferent fibers play an essential role in hypersensitivity from nerve damage Baron et al.
Furthermore, adrenergic sensitivity has extensively been expressed in complex regional pain syndromes II, post-traumatic neuralgias, and postherpetic neuralgias; while there is no sensitivity in the primary afferent neurons, which have been claimed in the case of polyneuropathies Schattschneider et al.
Therefore, sympathetically-induced and temperature-mediated pain can be cured by inhibiting their relevant receptors on nociceptive neurons. Ectopic activity is mediated by inflammation in both injured and contiguous typical primary afferent nociceptors, which are activated by nerve damage that generates proinflammatory cytokines, particularly tumor necrosis factor-α TNF-α Sommer, Furthermore, deep proximal, as well as paroxysmal pains are noticeable symptoms in the case of patients who have peripheral neuropathies, including human immunodeficiency virus-neuropathy.
Increased concentrations of proinflammatory cytokines and cyclooxygenase-2 COX-2 have been found in the nerve biopsy specimens of these patients Lindenlaub and Sommer, CNS forms precise anatomical connections with the thalamus, brain stem, cortex, and spinal cord.
Furthermore, these relations can connect the sensations that are produced in the high threshold primary afferents with the cortical areas of the CNS, which subsequently processes it into final painful sensations Woolf, The constant hyperactivity is produced by damaged nerves that are considered to be a causative factor for central sensitization, as well as triggering activity-dependent synaptic flexibility occurring inside the cortex.
Moreover, various factors are involved in central sensitization such as excitatory amino acid, changes in ion channel kinetics, different synaptic modulators, pre- and post-synaptic activation of kinases, and increased bulk of ionotropic receptors.
Most of the patients who have peripheral as well as central neuropathy demonstrate dominant synaptic facilitation leading to hypersensitivity and allodynia Campbell and Meyer, Additionally, peripheral nerve damage results in pre-synaptic changes such as alterations in the synthesis of neuromodulators, neurotransmitters, and modifications in the calcium channels density Hendrich et al.
In contrast, post-synaptic changes take place due to the increased density of receptors on account of increased synthesis of ion channels and scaffold proteins and the phosphorylation of N-methyl-D-aspartate NMDA subunits Cheng et al.
These alterations also lead to aberrant expression of the mitogen-activated protein kinase system and Nav 1. Furthermore, pathologically sensitized C-fibers sensitize neuropeptide substance P as well as a spinal dorsal horn SDH through the release of glutamate, which cannot be neglected.
Subsequently, glutamate demonstrates an excitatory action by acting upon the postsynaptic NMDA receptor contributing to central sensitization Ultenius et al. It has been observed that the involvement of loss of function of tonic γ-amino butyric acid-A GABA A -conciliated inhibition and enhanced excitatory neurotransmitters are caused by an induction of central sensitization, leading to peripheral hypersensitivity, specifically hyperalgesia and allodynia Knabl et al.
When this sensitivity is developed, the generally harmless tactile stimuli can trigger Aβ as well as Aδ low threshold mechanoreceptors Tal and Bennett, The most abundant inhibitory neurotransmitter in the brain is GABA Uddin et al.
GABA regulates diverse physiological functions such as anxiety, sleep, reward, and memory formation Zeilhofer et al.
Previously, it has been described that the role of inhibitory neurons, especially in SDH, act and monitor transmission of pain via the periphery to greater intensities of the brain Melzack and Wall, GABA, releasing from presynaptic neurons, acts postsynaptically with several receptors; G protein-coupled channels, GABA A, GABA B, as well as GABA C, are ligand-gated ion channels Gavande et al.
Generally, ionotropic GABA A receptors are comprised of 5 heteropentameric subunits that form transmembrane protein complexes Uddin and Rashid, Meanwhile, the α 1 β 2 γ 2 subunit is thought to be the most dominant one in the human brain Wafford, GABA initiation stimulates the membrane penetrability to chloride and carbonate ions that produce a net inner flow of anions as well as resulting in hyperpolarization.
Therefore, this hyperpolarizing post-synaptic reaction is known as inhibitory post-synaptic potential Semyanov et al. Physiologically, GABA-liberating interneurons impose a robust inhibitory regulation through dorsal horn neuronal cells. Besides, damage of these neurons might additionally stimulate the dominant sensitization of the models of peripheral partial nerve injury.
In rodents, injury caused the reduction of GABA release from the spine, with reduced GABA-producing glutamic acid decarboxylase Moore et al. However, in diseased conditions, an improved excitation state arises that is recognized as an enormous GABAergic neuronal loss or deterioration of interneurons.
It has been found that peripheral and central sensitization causes nerve injury and NP. GABAergic interneuronal loss is considered to be the main contributor to persistent pain states Bráz et al. In the spinal cord, pharmacological inhibition of GABAergic neurotransmission causes hyperalgesia and allodynia Gwak et al.
Likewise, GABA A receptor blockage could prompt a behavioral reaction, which was revealed by electrophysiological studies Hwang and Yaksh, Furthermore, the GABAergic system impaired chronic NP in animals Zeilhofer, As a result, spinal inhibitory neurotransmission may be appreciated as a pharmacological NP treatment.
Additionally, the crucial function of GABA in opioid-mediated antinociception has long been recognized Ossipov et al. Also, agonists of GABA A receptor-mediated antinociceptive activity have been recognized to stimulate or inhibit additional neurotransmitters McCarson and Enna, As a consequence, the agonists of the GABA receptor might play a dynamic role in considering chronic and acute pain McCarson and Enna, Incidentally, isoguvacine and muscimol, agonists of GABA A receptors, are described to oppose nerve injury-stimulated tactile allodynia Hwang and Yaksh, These receptors are strictly linked to huge diameter afferents involved in innocuous sensation Price et al.
Pharmacological as well as behavioral examinations have stated that a single or continuous intrathecal GABA response to spinal cord or GABA liberating cells reduce NP Eaton et al.
In addition, spinal GABA A receptors inhibition shows annoying peripheral nerve injury connected to hyperalgesia Yamamoto and Yaksh, In contrast, intrathecal administration of benzodiazepines BDZs and allosteric positive modulators of GABA A receptors have been extensively used in sleep complaints, convulsions, anxiety, and analgesic activity Tucker et al.
Even though it has analgesic properties, its usage in pain relief is limited due to sedation. Therefore, study is urgently needed in to GABAergic modulators which might play a prominent role in the attenuation of NP.
Flavonoids are polyphenolic compounds found in fruits, flowers, barks, grains, vegetables, roots, tea, stems, and so on Uddin et al.
Chemically, flavonoids are carbon skeletons comprising of two benzene rings A and B linked via a heterocyclic pyrane ring C Kumar and Pandey, as shown in Figure 2. Flavonoids can be divided into diverse subgroups according to the carbon of the C ring whereon the B ring is connected as well as the oxidation and degrees of unsaturation of the C ring Panche et al.
In , a novel constituent derived from an orange was believed to be a vitamin and called vitamin P. It was subsequently proved to be a flavonoid, rutin, that played an essential role in the isolation as well as the study of the mechanisms of several individual flavonoids.
In fact, several traditional medicines are mainly flavonoids. In past centuries, Tanacetum parthenium has been used as a prophylactic drug in the treatment of migraine, while Matricaria recutita , chamomile flowers, has been used as a tranquilizer for many decades, with both comprising of the active constituent apigenin Jäger et al.
Moreover, linden flowers, Tilia sp. Tiliaceae , have been used as sedative agents, and Calluna vulgaris might serve as a nerve-calming medicine, which has active components of kaempferol and quercetin Aguirre-Hernández et al.
Apart from the separation of natural flavonoids, several synthetic and semi-synthetic products have been synthesized and separated for their therapeutic potential Cushnie and Lamb, Up to now, diverse flavonoids have been isolated. Flavonoid compounds show different biological effects, such as neuroprotective Cho et al.
Flavonoids are widely targeted for their peripheral events; though, their selective affinity for GABA A receptors has extensively been demonstrated in studies using bovine and rat brain membrane binding analyses Hong and Hopfinger, Numerous behavioral tests have also widely been performed, which confirm the sedative effects of flavonoids in an animal model of anxiety that was devoid of the additional side effects of BDZs Griebel et al.
Remarkably, negative, positive, and neutral allosteric modulatory flavonoid actions of an extensive variety of ionotropic GABA receptors have been focused on and intensely supported through enormous evidence.
In the s, flavonoids had been well-defined as a novel family of BDZ receptor ligands Medina et al. Typically, they were believed to be acting upon BDZ receptors, as well as many synthetic flavonoids having a remarkable affinity for BDZ binding site Yao et al.
Moreover, GABA ratios were measured by the impact of ligand binding on the GABA binding site. These ratios displayed that flavones showed substantial biological actions at BDZ receptors Hanrahan et al.
GABA A receptors were enhanced by the flux of chloride ion that deliver a robust inhibitory effect via positive ionotropic modulators. As a result, these modulators are the strongest candidates for the management of CNS-associated diseases such as generalized anxiety, seizure disorders, sleep disturbances, panic disorders, muscle spasms, and NP Rudolph and Möhler, Furthermore, flavonoids might act upon a new binding site, excluding the classical BDZ binding site, which plays a pivotal role in searching for novel therapeutic candidates with limited adverse effects Rudolph and Möhler, Incidentally, 6-methoxyflavonone has been described to act as a positive allosteric modulator at α1β2γ2L and α2β2γ2L subunits of GABA A receptors Hall et al.
The substitution at 6-position on flavones is linked to its role in recombinant GABA A receptors. Furthermore, 6-methoxyflavone and 6-methoxyflavanone have been claimed to display anti-allodynic effects in cisplatin- and streptozotocin-stimulated NP models Akbar et al.
Therefore, these defensive properties against NP have been recognized to cause allosteric positive modulatory effects on opioid and GABA A receptors Akbar et al.
Additionally, myrcitin and baicalin exerted antiallodynic effects in sciatic nerve ligation models Cherng et al. Besides, quercetin and rutin have widely been claimed to suppress oxaliplatin-mediated chronic peripheral neuropathic pain Azevedo et al. Meanwhile, the antiallodynic potential of streptozotocin-induced painful diabetic neuropathy has been reported by naringin Kandhare et al.
Diabetic neuropathy is one of the most common causes of neuropathy and affects about million people in the world Boulton et al. Furthermore, genistein Valsecchi et al.
Moreover, MDA serves as a key biomarker for lipid damage as well as oxidative stress that can be caused by free radicals. In diabetic patients, the increased level of MDA has widely been observed in the serum as well as other tissues, which significantly affects the peripheral nerves Feldman et al.
Some flavonoids, such as genistein Valsecchi et al. Moreover, kaempferol decreased advanced glycation end products and epigallocatechin gallate EGCG causes a reduction of 8-hydroxydeoxyguanosine, which is considered as the major form of free radical-mediated oxidative stress in the nucleus and mitochondria Valavanidis et al.
It has also been found that in the diabetic animal model, genistein and naringenin raised nerve growth factor NGF in sciatic nerves Basu and Basu, Therefore, NGF servesas the survival and life maintenance of the neurons.
Table 1. Promising studies of flavonoids for the management of neuropathic pain. Diabetic neuropathy in animal models has widely been marked by evaluating behavioral signs, such as chemical, mechanical, thermal hyperalgesia, and tactile allodynia Pittenger et al.
It has also been observed that flavonoids considerably downregulated thermal, mechanical, chemical hyperalgesia, and tactile allodynia in diabetic animal models Figure 3. A number of flavonoids including fisetin Zhao et al.
Furthermore, fisetin Zhao et al. Numerous investigations have demonstrated that short term diabetes mediated mechanical, chemical, and thermal hyperalgesia Dyck et al. Besides, baicalein attenuated thermal hypoalgesia Stavniichuk et al.
The use of diverse chemotherapeutic agents and other anticancer drugs leads to the impairment of the peripheral nerves.
Chemotherapy-induced peripheral neuropathy CIPN is another form of neuropathy caused by anticancer drugs Hershman et al. Platinum compounds are extensively used in the management of several solid tumors. Oxaliplatin, a third-generation platinum agent, plays a pivotal role in diminishing antitumoral resistance with noticeable cytotoxicity Argyriou et al.
It has been observed that Azevedo et al. In a study by Schwingel et al. According to the study by Shahid et al. Hence, 6-methoxyflavone considerably reduced cisplatin-mediated mechanical allodynia by raising the paw withdrawal threshold as well as thermal hypoalgesia Figure 3 by improving the paw thermal threshold.
Chronic constriction injury CCI is considered to be the most extensively studied model for chronic neuropathic pain. There are various symptoms of CCI-induced pain including hyperalgesia, allodynia, paraesthesia, dysesthesia, and spontaneous pain Austin et al.
Flavonoids including hesperidin Carballo-Villalobos et al. In contrast, other flavonoids including genistein Valsecchi et al. As compared to morphine and gabapentin, quercetin decreased the mechanical and thermal hypersensitivities to a greater extent Çivi et al. When quercetin was administered in a pre-injury condition, it exerted long term actions on mechanical hypersensitivity, which further suggests the antinociceptive properties of quercetin in the CCI model Çivi et al.
Additionally, flavonoids including genistein Valsecchi et al. On the other hand, cold allodynia was reduced by morin Komirishetty et al. Although mechanical and cold hyperalgesia was reduced by luteolin, it did not affect thermal hyperalgesia Hara et al. However, thermal hyperalgesia was decreased by fisetin, but did not affect the nociceptive sensitivity to mechanical stimuli Zhao et al.
An elevated level of nitro oxidative stress can cause DNA damage, which can cause the activation of poly-ADP ribose polymerase PARP Figure 4 , which can further lead to PARP-induced DNA repair by transferring ADP-ribose units to the nuclear proteins. Nevertheless, activation of PARP can cause NF-κB activation, which can subsequently activate various inflammatory markers including interleukin IL -6, TNF-α, inducible nitric oxide synthase iNOS , and cyclooxygenase-2 COX-2 Obrosova et al.
Studies involving the CCI-induced neuropathic pain model revealed that flavonoids exert effects on various pro-inflammatory biomarkers Bertozzi et al. Furthermore, a single administration also decreased the expression levels of oligodendrocytes and microglia, whereas chronic treatment decreased astrocytes together with oligodendrocytes and microglia Bertozzi et al.
Puerarin decreased the elevated immunoreactivity of glial fibrillary acidic protein and ionized calcium-binding adaptor protein-1, which are astroglia and microglial activation markers, successively Liu et al. In the CCI-induced neuropathic pain model, morin decreased various inflammatory biomarkers including IL-6, TNF-α, phospho-NF-κB, NF-κB, COX-2, iNOS, and PARP Komirishetty et al.
Deoxyribonucleic acid DNA damage was found to be increased due to the CCI-induced nerve injury, which resulted in PARP overactivation Jagtap and Szabo, It was found that overactivation of PARP caused bioenergetic failure because overactivity of PARP requires a high amount of nicotinamide adenine dinucleotide NAD during DNA repair, and finally, NAD synthesis also requires adenosine triphosphate ATP , which can eventually lead to the disruption of biochemical processes that are dependent on ATP Hyo and Snyder, Figure 4.
Effects of flavonoids on peripheral neuropathy. Flavonoids act on different peripheral neuropathic pain conditions by blocking oxidative stress, activation of glial cells, and mitochondrial dysfunction. PARP, poly-ADP ribose polymerase. Treatment with morin caused marked restoration of CCI-mediated reduction in the ATP levels and also restored the neuronal cells from the bioenergetic crisis Komirishetty et al.
In a study, Kuang et al. It is known that TLR4 is a pattern recognition receptor and plays roles in the immune system and inflammatory diseases. When endogenous ligands bind with TLR4, it gets activated and stimulates the generation of pro-inflammatory cytokines by causing NF-κB activation Janeway and Medzhitov, ; Akira et al.
Furthermore, EGCG elevated the level of IL, reduced the downstream pro-inflammatory cytokines i. In the dorsal horn of the spinal cord, an EGCG-derived compound decreased the levels of mRNA and protein expressions of IL-6, NF-κB, IL-1β, and TNF-α Xifró et al.
Administration of isoorientin and puerarin also decreased the level of CCI-induced pro-inflammatory cytokines including IL-6, IL-1β, and TNF-α Liu et al.
Interestingly, genistein reduced the level of IL-1β expression in the spinal cord and dorsal root ganglion, while genistein also decreased mRNA expressions of both IL-6 and IL-1β in the sciatic nerve Valsecchi et al. Flavonoids show anti-inflammatory as well as antioxidant effects due to their action on GABA A receptors Hanrahan et al.
Maximum metabolic disorders are the result of oxidative stress. Along with exogenous factors, regular metabolism of oxygen inside the tissues and cells produce reactive oxygen species ROS and free radicals that steadily endanger them Forrester et al.
Flavonoids are well-recognized for their antioxidant properties and are also confirmed to show beneficial effects in several chronic diseases, including neurodegenerative disease, diabetes, atherosclerosis, and cancer de Teles et al.
Moreover, certain flavonoids play a crucial role in the iron chelation thus stopping the development of free radicals Nelson et al.
Rutin and epicatechin are shown to have the capability to be oxidized themselves through free radicals, producing a less reactive and stable species Hanasaki et al. Correspondingly, quercetin, a plant pigment flavonoid, prevents nitric oxide NO -mediated cell injury.
A combination of NO and free radicals generates the enormously injurious peroxynitrite, which directly oxidizes low-density lipoprotein and plays a crucial role in the permanent damage of the cell membrane.
Therefore, free radicals are scavenged by quercetin and restrained from reacting with NO, whereas, silibin reacts directly with NO Dehmlow et al.
Mechanical allodynia induced by spinal nerve ligation SNL was found to be decreased by various flavonoids including myricetin Hagenacker et al. SNL-induced thermal hyperalgesia was reduced by myricetin Hagenacker et al.
In addition to this, hesperetin and quercetin decreased partial sciatic nerve ligation-stimulated neuropathic pain and spared nerve injury Figure 3 ; Aswar et al.
Physiologically, xanthine dehydrogenase plays an important role in the metabolism of xanthine to uric acid, however, this enzyme alters into xanthine oxidase in the case of ischemic-reperfusion, which works as a precursor of free radicals.
There are various flavonoids, such as quercetin, silibinin, and luteolin, that are recognized to work as antioxidants through stopping xanthine oxidase Chang et al. Similarly, reperfusion is also caused by the mobilization of leucocytes producing the subsequent release of inflammatory mediators as well as cytotoxic oxidants, which provokes the complement system.
Many flavonoids play a key role in the immobilization of leucocytes, eventually resulting in a decline in the serum complement system as well as inflammation Friesenecker et al. It has been observed that the connection of the same pathophysiological mechanisms takes place with both NP of peripheral origin and inflammation.
Both kinds of pathologies express as hyperalgesia and allodynia Clatworthy et al. Moreover, inflammatory cells infiltration and their main secretory products, including cytokines and arachidonic acid, affect peripheral nerve damage, which is accountable for the production and maintenance of the constant pain Tracey and Walker, ; Cui et al.
When cytokines such as IL-1, IL-6, and TNF-α were injected into a rat paw, it would result in the initiation of thermal and mechanical hyperalgesia Cunha et al.
On the other hand, the inhibition of TNF-α in the animal models with painful neuropathy led to the reduction of hyperalgesia Sommer et al. The release of cytokines also activates COX-2 dependent prostanoid releases. Furthermore, prostaglandins PGs also play a pivotal role in triggering inflammation that increases sensitivity to pain Uddin et al.
It had been found that intrathecal injection of PGs such as PGE 2 and PGF 2α triggered allodynia in conscious mice Minami et al. Additionally, synthesis of NO and PG through COX-2 as well as iNOS is increased in the microglia on account of peripheral nerve damage, leading to hypersensitization Hanisch, It is evident that flavonoids show anti-inflammatory activity both in vitro and in vivo.
One of the imperative mechanisms of anti-inflammatory action is recognized by inhibiting eicosanoid producing enzymes such as phospholipase A2, lipoxygenases, and COX Kim et al.
Along with anti-inflammatory activity, flavonoids also block arachidonic acid metabolism Ferrándiz and Alcaraz, In this review, we discuss the effects of flavonoids in improving different NP conditions and how flavonoids control diverse pain biomarkers in animal models of NP.
Allosteric modulators at GABA A receptors can alter either the affinity or efficacy of agonists including GABA, subsequently controlling their activity. Flavonoids are strong allosteric modulators and may serve as valuable candidates in the management of NP. Hence, it can be said that there is huge potentiality in flavonoids for the development of novel therapeutics agents for NP, however, further studies are needed.
MU conceived the original idea and designed the outlines of the study. MU, AM, MR, and MK wrote the draft of the manuscript.
MU and AM prepared the figures for the manuscript. SA, IA, AP, GA, MB-J, and MA-D revised and improved the draft. All authors have read and approved the final manuscript. 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.
This work was funded by the Deanship of Scientific Research at Princess Nourah bint Abdulrahman University, through the Fast-track Research Funding Program.
BDZ, benzodiazepines; CNS, central nervous system; CIPN, chemotherapy-induced peripheral neuropathy; CCI, chronic constriction injury; EGCG, epigallocatechin gallate; GABA, γ -amino butyric acid; MDA, malondialdehyde; NMDA, N-methyl -D-aspartate; NP, neuropathic pain; NF- κ B, nuclear factor kappa B; Nrf2, nuclear factor erythroid 2-related factor 2; SDH, spinal dorsal horn; SNL, spinal nerve ligation; SSNS, somatosensory nervous system.
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Boulton, A. Guidelines for the diagnosis and outpatient management of diabetic peripheral neuropathy. Feverfew contains compounds that may reduce inflammation and muscle spasms. Some researchers believe that the key active compounds include sesquiterpene lactones and flavonoids.
The American Migraine Foundation states that there are mixed results about how effective feverfew is, but that it is probably helpful for preventing migraine headaches.
A study concludes that feverfew may have anti-inflammatory, antioxidant, and neuroprotective effects. Feverfew can cause side effects such as nausea, digestive problems, and bloating.
So, it is important to talk with a qualified healthcare professional before trying feverfew. Curcuma, the active ingredient in the spice turmeric , has pain-relieving qualities. A review claims that curcumin shows a reduction in pain similar to that of Nonsteroidal anti-inflammatory drugs NSAIDs.
However, researchers recommend turmeric as a safe adjunction to NSAID therapy rather than in place of it. Turmeric is also a common herbal remedy for reducing inflammation.
To include turmeric in its natural form in the diet, a person could try adding it to curries, smoothies, or juices. Acupuncture is an alternative therapy that advocates believe can help reduce pain.
Recent research supports these beliefs. The National Center for Complementary and Integrative Health NCCIH states that acupuncture can help with certain types of pain, including:.
It may also reduce how frequently people get tension headaches and could help prevent migraine headaches. A meta-analysis found that acupuncture is an effective way to manage chronic pain. The researchers concluded that acupuncture could help with musculoskeletal pain, headache, and pain associated with osteoarthritis.
More research into the effects of acupuncture for other pain conditions is now needed, but increasing evidence is suggesting that acupuncture is effective for many types of pain. In fact, acupuncture may help in more than different conditions.
Yoga is a physical meditation practice that may offer a way to manage pain naturally. Managing back pain often includes stretching and physical therapy. Yoga provides this.
It incorporates breathing exercises , self-care, and relaxation methods, so practicing yoga may also relieve pain related to stress or anxiety. A study found that 12 weeks of yoga helped to significantly reduce lower back pain. The NCCIH states that yoga may help relieve lower back pain and neck pain, but that there is not enough evidence that it can help for other conditions, such as headache, arthritis, or fibromyalgia.
People experiencing chronic pain are increasingly turning to mindfulness meditation as a natural treatment. More research is needed, but initial studies are promising.
A systematic review and meta-analysis looked at 38 studies and eventually concluded that mindfulness meditation can improve pain symptoms, depression, and quality of life. However, the authors say that larger studies are needed to see exactly how effective it is. Essential oils, such as lavender oil and peppermint oil, may relieve pain naturally.
This is also the case for certain herbs such as clove and feverfew. Acupuncture, yoga, and mindfulness meditation are thought to be natural pain relievers too. Relaxation techniques, breathing exercises, and heat and cold treatment can be home remedies that alleviate pain quickly.
When a person takes traditional pain relief medication as prescribed, with guidance from a qualified healthcare professional, it is a safe and effective way to manage pain. Natural pain relievers, however, offer an alternative for people who want to avoid the long term side effects of pain relief medication.
People can use essential oils by adding a few drops to a tissue or a steam bath and inhaling the vapor. People can also add the herbs and spices listed above to food.
However, if a person is unable to do that, they can instead take them as supplements. Not every natural pain reliever will work for everyone. Some people may find that a natural option that works well for them in the long term.
Others may not be able to manage pain naturally and may prefer traditional medication. Anyone with severe pain, including pain related to an existing health condition, should speak with a qualified healthcare professional.
They can advise how best to manage this. Chronic pain is complex, and it can take some time to work out the best methods for pain relief. Modern Plant Physiology. Applied and Environmental Microbiology. Bibcode : ApEnM.. Metabolic Engineering. Part II: Reconstruction of multienzyme pathways in plants and microbes".
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Biotechnology Letters. Andersen ØM, Markham KR Grotewold E The science of flavonoids. New York: Springer. Harborne JB Comparative Biochemistry of the Flavonoids.
g Journal of Molecular Structure. Wikimedia Commons has media related to Flavonoids. Types of flavonoids. Apigenin , Chrysin , et. Quercetin , Kaempferol , et. Daidzein , Genistein , Orobol et. Catechin , Gallocatechol , et.
Apiforol , Luteoforol , et. Leucocyanidin , Leucodelphinidin , et. Hesperidin Naringenin Eriodictyol. Taxifolin Aromadendrin , et. Cyanidin , Delphinidin , et. Apigeninidin , Guibourtinidin , et. Aureusidin Leptosidin. Butein , Isoliquiritigenin , et.
List of phytochemicals in food C-methylated flavonoids O-methylated flavonoids Furanoflavonoids Pyranoflavonoids Prenylflavonoids Methylenedioxy Castavinols.
Flavonoid biosynthesis. Types of phenylpropanoids. Hydroxycinnamic acids Chromones Furanochromones Cinnamaldehydes Monolignols Coumarins Chalcones Flavonoids Allylbenzenes Stilbenoids Lignans Lignins Suberins. Types of phenolic compounds.
Benzenediols Benzenetriols Apiole Carnosol Carvacrol Dillapiole Rosemarinol. Types of polyphenols. Matairesinol Secoisolariciresinol Pinoresinol. Resveratrol Pterostilbene Piceatannol Pinosylvin. Types of natural tannins. Punicalagins Castalagins Vescalagins Castalins Casuarictins Grandinins Punicalins Roburin A Tellimagrandin IIs Terflavin B.
Digalloyl glucose 1,3,6-Trigalloyl glucose. Proanthocyanidins Polyflavonoid tannins Catechol-type tannins Pyrocatecollic type tannins Flavolans. Epicutissimin A Acutissimin A. Tannin sources Pseudo tannins Synthetic tannins Tannin uses Enological Drilling Ink Tanning. Diarylheptanoids C6-C7-C6 Anthraquinones Chalconoids C6-C3-C6 Kavalactones Naphthoquinones C6-C4 Phenylpropanoids C6-C3 Xanthonoids C6-C1-C6 Coumarins and isocoumarins.
Aromatic acids. p-Hydroxybenzoic acid glucoside. Bergenin Chebulic acid Ethyl gallate Eudesmic acid Gallic acid Tannic acid Norbergenin Phloroglucinol carboxylic acid Syringic acid Theogallin. Vanillin Ellagic acid. α-Cyanohydroxycinnamic acid Caffeic acid Chicoric acid Cinnamic acid Chlorogenic acid Diferulic acids Coumaric acid Coumarin Ferulic acid Sinapinic acid.
phenylalanine tryptophan histidine tyrosine thyroxine 5-hydroxytryptophan L-DOPA. Tyrosol Hydroxytyrosol Oleocanthal Oleuropein. Capsaicin Gingerol Alkylresorcinols. Phenolic compounds Phlorotannins. Authority control databases : National Spain France BnF data Germany Israel United States Latvia Japan Czech Republic.
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There are various natural ways to cure, narural, or relieve pain. Ss include essential oils, herbal Citrus fruit varieties, and other batural and alternative Flavonoids as natural pain relievers. People have Flavoonids essential oils, Flavonoids as natural pain relievers, and alternative therapies as natural pain relievers for hundreds of years. Researchers have not fully explored these options, but some evidence suggests that certain remedies can help and that many people find them useful. In this article, we discuss 12 natural pain relievers and the science behind them. Read on to learn how to manage pain naturally without relying on over-the-counter pain medication. Pain due to chronic rellievers is Flavonoods frequent ax insufficiently addressed problem. Current drug options for pain management either Flavonoids as natural pain relievers cases of chronic inflammatory Flavonoidds or neuropathy do not Flavonoidx treat Mineral-rich supplements. Flavonoids as natural pain relievers, they are associated with important adverse events in long term use. Luteolin is a flavonoid widely present in the plant kingdom and its sources have been assembled in a comprehensive list of this paper. Luteolin has shown in several research studies a range of pharmacological properties; anti-inflammatory, antioxidant, neuroprotective, and analgesic. In this article, we summarize the effects and potential benefits from introducing luteolin as an adjuvant agent in established protocols for pain management. We review the most indicative in vivo and in vitro evidence of how luteolin can target the molecular pathways involved in pathogenesis of chronic inflammatory and neuropathic pain.
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