Herbal Plants with Potential Anti-arthritic Activities via Nf Kb rheumatoid (Lawrence, 2009). Consistently, NF-κB activation has been demonstrated in the synovial tissue of RA patients, and this appears to be related to the clinical manifestation. Uncontrolled regulation of proteins that direct the NF-kB pathway is likely to contribute to the susceptibility or severity of chronic inflammatory diseases (Lawrence, 2009). Say no to plagiarism. Get a tailor-made essay on “Why violent video games should not be banned”? Get the original essay The joints of rheumatic patients are characterized by synovial infiltration of immune cells, leading to chronic inflammation, pannus formation and damage articular and cartilaginous that result. The RA synovium is known to have predominantly macrophages (30-40%), T cells (~30%), and synovial fibroblasts, as well as B cells, dendritic cells, other immune cells, and synovial structures such as the endothelium (Choy, 2012; Gibofsky, 2012.). RA synovial fluid has been analyzed and contains a wide variety of effector molecules, including pro-inflammatory cytokines (such as IL-1ß, IL-6, TNFa and IL-18), chemokines (such as IL-8, IP-10, MCP-1, MIP). -1 and RANTES), matrix metalloproteinases (MMPs, such as MMP-1, -3, -9 and -13) in addition to metabolic proteins (such as Cox-1, Cox-2 and iNOS) (Herkenham M., 2011 ).These are correlated in a complex way that is thought to cause a vicious cycle of pro-inflammatory signals leading to frequent and chronic inflammation. TNFa is obviously the key mediator of inflammation and also induces apoptosis. Importantly, genes encoding TNFa and many other listed factors are well known to be under the control of NF-kB transcription factors, suggesting that NF-kB may be a master regulator of production of inflammatory cytokines in RA. Indeed, the existence of activated NF-kB transcription factors has been verified in synovial fibroblasts in culture (Hayden MS., 2011. -). Human arthritic joints and joints of animals with experimentally induced RA. Immunohistochemistry demonstrated the presence of both p50 and p65 in the nuclei of cells lining the synovial membrane and macrophages (Giopanou I., 2014). Additionally, nuclear extracts of cells verified an ability to bind the NF-kB consensus sequence. Recent practice such as in vivo imaging has also been used to demonstrate NF-kB activity in a mouse model of chronic inflammation. By placing the luciferase gene under the control of NF-βB, a marked increase in luminescence was observed in the joints of mice (Mann, 2002.). These results are supported by a study investigating experimentally induced arthritis in mice carrying knockout genes for the NF-kB family member p50 or c-Rel. The two experimental models used were collagen-induced arthritis (a model of chronic RA where disease development involves both T and B cells) and an acute/destructive model induced by BSA and IL- 1 methylated (exclusively involving T cells). The fruit of CapsicumCapsicum annum has been used traditionally by natives of the American tropics for many centuries. It was originally cultivated in the tropics ofUnited States of America. It is known to contain high chemicals that cause highly selective anesthesia through the degradation of capsaicin-sensitive nociceptive nerve endings. It is known to be potent in activating the vanilloid-1 receptor potential. It is believed to be the primary receptor for nociception. It is also suggested to have the ability to inhibit NF-kB activation as a mechanism of action to generate the anti-inflammatory effect. The herb is often mixed with other natural herbal anti-arthritic preparations. It is also used for peripheral neuronal disorders and chronic musculoskeletal pain (Caterina MJ; SurhYJ).Turmeric SPPS Several members of the genus Curcuma are used in traditional medicine, the most important being Curcuma longa (CL); turmeric. Its rhizome has been used for centuries as a dietary spice as well as an herb for its anti-inflammatory properties, hence its usefulness in arthritic diseases, including RA (Sharma, 2006b). Animal studies. In an animal arthritis model, a CL preparation lacking essential oil strongly suppressed joint inflammation and periarticular damage correlating with a decrease in NF-kB activation and cascade of events (involving mediators of inflammation and injury such as chemokines, cyclooxygenase 2, and receptor activator of nuclear factor kappa-B ligand (Funk, 2006). The ability to prevent destructive changes in joints and periarticular bones appears to be comparable to that of betamethasone (Kamarudin, 2012; Taty Anna, 2011). bone building, while stopping the progression of osteoarthritis (Chang, 2015). In a rat model of induced arthritis, application of ginger and turmeric rhizomes was better than indomethacin (a potent NSAID). terms of ability to improve both joint histopathological changes and extra-articular manifestations, including systemic inflammation, malnutrition and iron deficiency anemia, without intolerance to renal function and reduced risk of cardiovascular disease (Ramadan, 2013) .In human clinical studies, a combination of Curcuma longa and Boswellia serrata was found to be more effective than a standard dose of celecoxib (a selective COX-2 inhibitor) in the treatment of osteoarthritis, thereby improving the the patient's condition, without detectable toxicity by clinical examination and laboratory tests (Kizhakkedath, 2013). Curcuma domestica extracts have been shown to be useful in knee osteoarthritis, reducing pain and functionally with equivalent effectiveness to ibuprofen, but with fewer side effects (Kuptniratsaikul, 2014). A recent meta-analysis found relevant scientific evidence for the effectiveness of turmeric as a therapeutic option for arthritis, but concluded that additional studies are needed to definitively pin it down (Daily, 2016). Diferuloylmethane is the active ingredient phenolic pigment. commonly known as curcumin, which has a complex beneficial action in various areas of pathology due to its ability to favorably influence various signaling pathways and mediators (Ghosh, 2015). In a rat model of arthritis, it was shown to improve joint inflammation, being even more effective in the first hours after the arthritis-inducing event than a low dose of prednisone (Nonose, 2014).AilIt is well established that IL-1ß, once bound to its type 1 receptor, activates NF-βB dimers by triggering thephosphorylation and subsequent degradation of IβB inhibitory proteins. Activation of NF-βB was a requirement for IL-1ß-induced MMP-13 secretion in OA chondrocytes (Kim SR, 2013.) (Tsutsumi R., 2008.). Also, Imamura et al. proved that IL-1ß and TNF-a inhibited chondrogenesis via the NF-βB pathway in human mesenchymal stem cells (Imamura M., 2014). Various garlic products have been studied in the treatment of osteoarthritis (Williams FMK, 2010). A sulfur compound isolated from garlic was shown to suppress arthritis by inhibiting the DNA binding activity of NF-?B and the expression of iNOS and COX-2 (Ban JO, 2009 .). However, there are a few studies on the effect of SAMC on osteoarthritis. Furthermore, a previous study found that DATS suppressed MMP2-9 expression which depended on NF-?B and ERK-MAPK signaling pathways (Liu Y., 2015). Mechanistically, SAMC was found to be linked to increased levels of IL-1ß-induced I?Ba, which subsequently attenuated p65 nuclear translocation and NF-?B transcriptional activity. Furthermore, our results indicated that IL-1ßa treatment led to a significant increase in TNF-a expression at the mRNA and protein levels, which was enhanced by SAMC treatment. The combination of these results suggests that SAMC can potentially be applied in the treatment of osteoarthritis. GingerZingiber officinalis, also known as ginger, is a commonly used spice in Asian cuisine and a traditional remedy for joint diseases in ethnomedicine (Sharma, 2006a). Ginger is thought to have anti-inflammatory effects, probably by inhibiting COX-1, COX-2 and LOX (Grzanna, 2005, ). Nevertheless, pressed ginger extract paradoxically increased the synthesis of pro-inflammatory cytokines (TNF-a, IL-6 and monocyte chemoattractant protein-1) in RAW264 cell culture (Ueda, 2010). Oral administration of ginger extract had a dual effect on the synthesis of TNF-a in mice, in peritoneal cells: ZO extract initially increased it, but with repeated administrations reduced it. (Ueda, 2010). Additionally, it increased serum corticosterone level, which might contribute to the anti-inflammatory effect of ZO. A recent human clinical study found that supplementing with ZO powder for three months can reduce serum levels of nitric oxide and high-sensitivity reactive proteins. hs-CRP in patients with knee osteoarthritis. Inflammatory markers began to decrease after three weeks of treatment (Naderi, 2016). Several other studies have shown clinical improvement in osteoarthritis patients with ZO extract, assessed by VAS pain score, reduction in rescue medication use, mostly mild gastrointestinal adverse events, and an effectiveness and satisfaction score similar, or even better, to that of the standard prescribed treatment. by the orthopedic specialist. ZO's pungent-tasting constituents are believed to contribute to the anti-inflammatory activity of this medicinal plant. For example, ginger inhibited κB kinase activity required for NF-κB activation and suppressed NF-κB-regulated expression of inflammatory genes in lipopolysaccharide S-activated macrophages (Lee, 2012). ). 6-Dehydrogingerdione attenuated the gene expression of iNOS, COX-2, IL-1ß, IL-6 and TNF-a in vitro, in RAW 264.7 macrophages. (Huang, 2014, ).LicoriceApproximately 300 polyphenols have been isolated from licorice, including phenolic acids, flavonoids, flavans, chalcones, isoflavans and isoflavonoids. So far, the main anti-inflammatory active polyphenols in licorice are chalcones, isoflavans andisoflavonoids. The mechanisms of the anti-inflammatory activities of chalcones have been fully investigated. LCA, LCB, ISL, and EC all inhibited the production of NO, IL-6, and PGE2, while LCA, LCB, and LCD all exhibited potent inhibition of lipid peroxidation (Fu Y, 2013.) (Honda H, 2014. ). Both LCB and LCD strongly inhibited the production of superoxide anions in the xanthine oxidase system, showed potent scavenging activity on the DPPH radical, and inhibited the phosphorylation of NF-?B p65 (Furusawa J, 2009.). Furthermore, LCC decreased the expression and activity of iNOS, and modulated the activity of the antioxidant network of SOD, catalase and glutathione peroxidase (Wang Z, 2013.). LCE effectively inhibited PKC/JNK, ERK1/2, reduced the expression of iNOS, COX-2, IL-6, IL-1ß, IL-12p40, TNF-a, AKT and p38, mitogen-activated protein kinase ( MAPK), and attenuated I?Ba degradation and NF-?B activities, as well as the transcriptional activity of AP-1 activator protein (Cho YC, 2010. ) (Lee HN, 2013. ). Besides chalcones, other flavonoids present in licorice, including DGC, DGD, ISOA, GLD, LID, and LIA, have also shown excellent anti-inflammatory activities. DGC, DGD, and ISOA all showed strong ferric reducing activities and effectively removed DPPH, ABTS+, and singlet oxygen radicals (Kim HJ, 2012). Moreover, DGC increased the expression of hemeoxygenase-1 and MAPK phosphatase-1, suppressed inflammation-mediated neurodegeneration, production of TNF-a, NO, ROS, NF-βB and phosphorylation of p38 MAPK, ERK1/2, IβBa. and p65 (Kim J, 2013. ).GLD significantly inhibited the release of NO and IL-1ß (Thiyagarajan P, 2011. ), attenuated colonic inflammation in mice with sulfate-induced colitis of dextran sodium and decreased iNOS mRNA expression under high glucose levels, indicating that GLD could be applied to diabetes-related vascular dysfunction (Yehuda I, 2015.). LID and LIA inhibited the secretion of IL-6, chemokine ligand 5 (CC motif), MMP-7, -8 and -9. Suppression of cytokine and MMP secretion by LID and LIA has been associated with reduced activation of NF-?B p65 in the treatment of periodontitis (La VD, 2011. ).GranadaAs mentioned above, studies in vivo have defined a clear role for NF-kB in the modulation of inflammation by pomegranate extracts, a finding which appears to be confirmed in vitro. Pomegranate juice (Velagapudi, 2016), POMxTM extract (Rasheed, 2009) and their bioactive compounds punicalagin (YEH Kim, CJ; Lee, HP; Kim, CS; Son, DJ; Ham, YW; Hellström, M.; Han , SB; Kim, HS; Park, EK 2017, ) or delphinidin (Seong, 2011) all suppressed NF-kB activation in various cell types. ET was found to reduce NF-kB target expression. genes, including IL-6 and interleukin 8 (IL-8), upon exposure to pro-inflammatory stimuli in intestinal cells (Hollebeeck, 2012, ), while EA (Promsong, 2015, ) and POMxTM (Rasheed, 2009 #187) reduced NF-kB activation in various immune cell subsets and the anthocyanin delphinidin reduced inflammation in rheumatoid arthritis cells (Seong, 2011). Taken together, these results suggest that ET and other bioactive compounds present in pomegranate juice exhibit anti-inflammatory effects in vitro and that the mechanisms involved appear to be related to inactivation of NF-kB signaling. The administration of products derived from pomegranate has been demonstrated. to reduce local inflammation in the bronchoalveolar tissue of COPD model mice (Husari, 2016) and in the joints of RA model mice (Shukla, 2008,). There is also ample evidence to suggest that pomegranate extract exerts anti-inflammatory effects..

Essay / Herbal Plants with Potential Anti-arthritic Activities via Nf Kb rheumatoid (Lawrence, 2009). Consistently, NF-κB activation has been demonstrated in the synovial tissue of RA patients, and this appears to be related to the clinical manifestation. Uncontrolled regulation of proteins that direct the NF-kB pathway is likely to contribute to the susceptibility or severity of chronic inflammatory diseases (Lawrence, 2009). Say no to plagiarism. Get a tailor-made essay on “Why violent video games should not be banned”? Get the original essay The joints of rheumatic patients are characterized by synovial infiltration of immune cells, leading to chronic inflammation, pannus formation and damage articular and cartilaginous that result. The RA synovium is known to have predominantly macrophages (30-40%), T cells (~30%), and synovial fibroblasts, as well as B cells, dendritic cells, other immune cells, and synovial structures such as the endothelium (Choy, 2012; Gibofsky, 2012.). RA synovial fluid has been analyzed and contains a wide variety of effector molecules, including pro-inflammatory cytokines (such as IL-1ß, IL-6, TNFa and IL-18), chemokines (such as IL-8, IP-10, MCP-1, MIP). -1 and RANTES), matrix metalloproteinases (MMPs, such as MMP-1, -3, -9 and -13) in addition to metabolic proteins (such as Cox-1, Cox-2 and iNOS) (Herkenham M., 2011 ).These are correlated in a complex way that is thought to cause a vicious cycle of pro-inflammatory signals leading to frequent and chronic inflammation. TNFa is obviously the key mediator of inflammation and also induces apoptosis. Importantly, genes encoding TNFa and many other listed factors are well known to be under the control of NF-kB transcription factors, suggesting that NF-kB may be a master regulator of production of inflammatory cytokines in RA. Indeed, the existence of activated NF-kB transcription factors has been verified in synovial fibroblasts in culture (Hayden MS., 2011. -). Human arthritic joints and joints of animals with experimentally induced RA. Immunohistochemistry demonstrated the presence of both p50 and p65 in the nuclei of cells lining the synovial membrane and macrophages (Giopanou I., 2014). Additionally, nuclear extracts of cells verified an ability to bind the NF-kB consensus sequence. Recent practice such as in vivo imaging has also been used to demonstrate NF-kB activity in a mouse model of chronic inflammation. By placing the luciferase gene under the control of NF-βB, a marked increase in luminescence was observed in the joints of mice (Mann, 2002.). These results are supported by a study investigating experimentally induced arthritis in mice carrying knockout genes for the NF-kB family member p50 or c-Rel. The two experimental models used were collagen-induced arthritis (a model of chronic RA where disease development involves both T and B cells) and an acute/destructive model induced by BSA and IL- 1 methylated (exclusively involving T cells). The fruit of CapsicumCapsicum annum has been used traditionally by natives of the American tropics for many centuries. It was originally cultivated in the tropics ofUnited States of America. It is known to contain high chemicals that cause highly selective anesthesia through the degradation of capsaicin-sensitive nociceptive nerve endings. It is known to be potent in activating the vanilloid-1 receptor potential. It is believed to be the primary receptor for nociception. It is also suggested to have the ability to inhibit NF-kB activation as a mechanism of action to generate the anti-inflammatory effect. The herb is often mixed with other natural herbal anti-arthritic preparations. It is also used for peripheral neuronal disorders and chronic musculoskeletal pain (Caterina MJ; SurhYJ).Turmeric SPPS Several members of the genus Curcuma are used in traditional medicine, the most important being Curcuma longa (CL); turmeric. Its rhizome has been used for centuries as a dietary spice as well as an herb for its anti-inflammatory properties, hence its usefulness in arthritic diseases, including RA (Sharma, 2006b). Animal studies. In an animal arthritis model, a CL preparation lacking essential oil strongly suppressed joint inflammation and periarticular damage correlating with a decrease in NF-kB activation and cascade of events (involving mediators of inflammation and injury such as chemokines, cyclooxygenase 2, and receptor activator of nuclear factor kappa-B ligand (Funk, 2006). The ability to prevent destructive changes in joints and periarticular bones appears to be comparable to that of betamethasone (Kamarudin, 2012; Taty Anna, 2011). bone building, while stopping the progression of osteoarthritis (Chang, 2015). In a rat model of induced arthritis, application of ginger and turmeric rhizomes was better than indomethacin (a potent NSAID). terms of ability to improve both joint histopathological changes and extra-articular manifestations, including systemic inflammation, malnutrition and iron deficiency anemia, without intolerance to renal function and reduced risk of cardiovascular disease (Ramadan, 2013) .In human clinical studies, a combination of Curcuma longa and Boswellia serrata was found to be more effective than a standard dose of celecoxib (a selective COX-2 inhibitor) in the treatment of osteoarthritis, thereby improving the the patient's condition, without detectable toxicity by clinical examination and laboratory tests (Kizhakkedath, 2013). Curcuma domestica extracts have been shown to be useful in knee osteoarthritis, reducing pain and functionally with equivalent effectiveness to ibuprofen, but with fewer side effects (Kuptniratsaikul, 2014). A recent meta-analysis found relevant scientific evidence for the effectiveness of turmeric as a therapeutic option for arthritis, but concluded that additional studies are needed to definitively pin it down (Daily, 2016). Diferuloylmethane is the active ingredient phenolic pigment. commonly known as curcumin, which has a complex beneficial action in various areas of pathology due to its ability to favorably influence various signaling pathways and mediators (Ghosh, 2015). In a rat model of arthritis, it was shown to improve joint inflammation, being even more effective in the first hours after the arthritis-inducing event than a low dose of prednisone (Nonose, 2014).AilIt is well established that IL-1ß, once bound to its type 1 receptor, activates NF-βB dimers by triggering thephosphorylation and subsequent degradation of IβB inhibitory proteins. Activation of NF-βB was a requirement for IL-1ß-induced MMP-13 secretion in OA chondrocytes (Kim SR, 2013.) (Tsutsumi R., 2008.). Also, Imamura et al. proved that IL-1ß and TNF-a inhibited chondrogenesis via the NF-βB pathway in human mesenchymal stem cells (Imamura M., 2014). Various garlic products have been studied in the treatment of osteoarthritis (Williams FMK, 2010). A sulfur compound isolated from garlic was shown to suppress arthritis by inhibiting the DNA binding activity of NF-?B and the expression of iNOS and COX-2 (Ban JO, 2009 .). However, there are a few studies on the effect of SAMC on osteoarthritis. Furthermore, a previous study found that DATS suppressed MMP2-9 expression which depended on NF-?B and ERK-MAPK signaling pathways (Liu Y., 2015). Mechanistically, SAMC was found to be linked to increased levels of IL-1ß-induced I?Ba, which subsequently attenuated p65 nuclear translocation and NF-?B transcriptional activity. Furthermore, our results indicated that IL-1ßa treatment led to a significant increase in TNF-a expression at the mRNA and protein levels, which was enhanced by SAMC treatment. The combination of these results suggests that SAMC can potentially be applied in the treatment of osteoarthritis. GingerZingiber officinalis, also known as ginger, is a commonly used spice in Asian cuisine and a traditional remedy for joint diseases in ethnomedicine (Sharma, 2006a). Ginger is thought to have anti-inflammatory effects, probably by inhibiting COX-1, COX-2 and LOX (Grzanna, 2005, ). Nevertheless, pressed ginger extract paradoxically increased the synthesis of pro-inflammatory cytokines (TNF-a, IL-6 and monocyte chemoattractant protein-1) in RAW264 cell culture (Ueda, 2010). Oral administration of ginger extract had a dual effect on the synthesis of TNF-a in mice, in peritoneal cells: ZO extract initially increased it, but with repeated administrations reduced it. (Ueda, 2010). Additionally, it increased serum corticosterone level, which might contribute to the anti-inflammatory effect of ZO. A recent human clinical study found that supplementing with ZO powder for three months can reduce serum levels of nitric oxide and high-sensitivity reactive proteins. hs-CRP in patients with knee osteoarthritis. Inflammatory markers began to decrease after three weeks of treatment (Naderi, 2016). Several other studies have shown clinical improvement in osteoarthritis patients with ZO extract, assessed by VAS pain score, reduction in rescue medication use, mostly mild gastrointestinal adverse events, and an effectiveness and satisfaction score similar, or even better, to that of the standard prescribed treatment. by the orthopedic specialist. ZO's pungent-tasting constituents are believed to contribute to the anti-inflammatory activity of this medicinal plant. For example, ginger inhibited κB kinase activity required for NF-κB activation and suppressed NF-κB-regulated expression of inflammatory genes in lipopolysaccharide S-activated macrophages (Lee, 2012). ). 6-Dehydrogingerdione attenuated the gene expression of iNOS, COX-2, IL-1ß, IL-6 and TNF-a in vitro, in RAW 264.7 macrophages. (Huang, 2014, ).LicoriceApproximately 300 polyphenols have been isolated from licorice, including phenolic acids, flavonoids, flavans, chalcones, isoflavans and isoflavonoids. So far, the main anti-inflammatory active polyphenols in licorice are chalcones, isoflavans andisoflavonoids. The mechanisms of the anti-inflammatory activities of chalcones have been fully investigated. LCA, LCB, ISL, and EC all inhibited the production of NO, IL-6, and PGE2, while LCA, LCB, and LCD all exhibited potent inhibition of lipid peroxidation (Fu Y, 2013.) (Honda H, 2014. ). Both LCB and LCD strongly inhibited the production of superoxide anions in the xanthine oxidase system, showed potent scavenging activity on the DPPH radical, and inhibited the phosphorylation of NF-?B p65 (Furusawa J, 2009.). Furthermore, LCC decreased the expression and activity of iNOS, and modulated the activity of the antioxidant network of SOD, catalase and glutathione peroxidase (Wang Z, 2013.). LCE effectively inhibited PKC/JNK, ERK1/2, reduced the expression of iNOS, COX-2, IL-6, IL-1ß, IL-12p40, TNF-a, AKT and p38, mitogen-activated protein kinase ( MAPK), and attenuated I?Ba degradation and NF-?B activities, as well as the transcriptional activity of AP-1 activator protein (Cho YC, 2010. ) (Lee HN, 2013. ). Besides chalcones, other flavonoids present in licorice, including DGC, DGD, ISOA, GLD, LID, and LIA, have also shown excellent anti-inflammatory activities. DGC, DGD, and ISOA all showed strong ferric reducing activities and effectively removed DPPH, ABTS+, and singlet oxygen radicals (Kim HJ, 2012). Moreover, DGC increased the expression of hemeoxygenase-1 and MAPK phosphatase-1, suppressed inflammation-mediated neurodegeneration, production of TNF-a, NO, ROS, NF-βB and phosphorylation of p38 MAPK, ERK1/2, IβBa. and p65 (Kim J, 2013. ).GLD significantly inhibited the release of NO and IL-1ß (Thiyagarajan P, 2011. ), attenuated colonic inflammation in mice with sulfate-induced colitis of dextran sodium and decreased iNOS mRNA expression under high glucose levels, indicating that GLD could be applied to diabetes-related vascular dysfunction (Yehuda I, 2015.). LID and LIA inhibited the secretion of IL-6, chemokine ligand 5 (CC motif), MMP-7, -8 and -9. Suppression of cytokine and MMP secretion by LID and LIA has been associated with reduced activation of NF-?B p65 in the treatment of periodontitis (La VD, 2011. ).GranadaAs mentioned above, studies in vivo have defined a clear role for NF-kB in the modulation of inflammation by pomegranate extracts, a finding which appears to be confirmed in vitro. Pomegranate juice (Velagapudi, 2016), POMxTM extract (Rasheed, 2009) and their bioactive compounds punicalagin (YEH Kim, CJ; Lee, HP; Kim, CS; Son, DJ; Ham, YW; Hellström, M.; Han , SB; Kim, HS; Park, EK 2017, ) or delphinidin (Seong, 2011) all suppressed NF-kB activation in various cell types. ET was found to reduce NF-kB target expression. genes, including IL-6 and interleukin 8 (IL-8), upon exposure to pro-inflammatory stimuli in intestinal cells (Hollebeeck, 2012, ), while EA (Promsong, 2015, ) and POMxTM (Rasheed, 2009 #187) reduced NF-kB activation in various immune cell subsets and the anthocyanin delphinidin reduced inflammation in rheumatoid arthritis cells (Seong, 2011). Taken together, these results suggest that ET and other bioactive compounds present in pomegranate juice exhibit anti-inflammatory effects in vitro and that the mechanisms involved appear to be related to inactivation of NF-kB signaling. The administration of products derived from pomegranate has been demonstrated. to reduce local inflammation in the bronchoalveolar tissue of COPD model mice (Husari, 2016) and in the joints of RA model mice (Shukla, 2008,). There is also ample evidence to suggest that pomegranate extract exerts anti-inflammatory effects..

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