Index IntroductionCapsicumTurmeric SPPGarlicGingerLicoricePomegranateResveratrolConclusionIntroductionMany studies propose that NF-kB is essential for the expression of inflammatory cytokines and tissue-damaging enzymes in rheumatoid arthritis (Lawrence, 2009). Consistently, NF-kB activation has been demonstrated in synovial tissue of patients with rheumatoid arthritis and this appears to correlate with clinical manifestation. Uncontrolled regulation of proteins directing the NF-kB pathway likely contributes 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 Shouldn't Be Banned"? Get an original essayThe joints of rheumatic patients are characterized by synovial infiltration of immune cells, leading to chronic inflammation, pannus formation, and subsequent joint and cartilage damage. It is known that the RA synovium essentially possesses macrophages (30-40%), T cells (~30%) and synovial fibroblasts alongside B cells, dendritic cells, other immune cells and synovial cells such as the endothelium (Choy, 2012 ; Gibofsky, 2012.). RA synovial fluid was analyzed and contains a wide variety of effector molecules including proinflammatory cytokines (such as IL-1ß, IL-6, TNFα 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) as well as metabolic proteins (such as Cox-1, Cox-2 and iNOS) (Herkenham M ., 2011 ). These are interrelated in a complex way that is presumed to cause a vicious cycle of proinflammatory signals resulting in frequent and chronic inflammation. TNFα is obviously the key mediator of inflammation and also induces apoptosis. Importantly, genes encoding TNFα and many other listed factors are known to be under the control of NF-κB transcription factors, suggesting that NF-κB may be a master regulator of inflammatory cytokine production in rheumatoid arthritis. In fact, the existence of activated NF-kB transcription factors has been verified in synovial fibroblast cultures (Hayden MS., 2011. -). Human arthritic joints and animal joints with experimentally induced RA. Immunohistochemistry has demonstrated the presence of both p50 and p65 in the nucleic cells lining the synovial membrane and in macrophages (Giopanou I., 2014). Furthermore, cell nuclear extracts verified the ability to bind the NF-kB consensus sequence. A 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-?B, a marked increase in luminescence was observed in the joints of mice (Mann, 2002. ). These findings are supported by a study that investigated experimentally induced arthritis in mice carrying NF-kB family member p50 or c-Rel knockout genes. The two experimental models used were collagen-induced arthritis (a model of chronic rheumatoid arthritis in which disease development involves both T cells and B cells) and an acute/destructive model induced by methylated BSA and IL-1 ( involving exclusively T cells). The Capsicum fruitCapsicum annum has been used traditionally by natives of the American tropics for many centuries. It was originally grown in the tropics of the United States of America. It is known to contain high chemicals that cause highly selective anesthesia by disrupting nociceptive nerve endings sensitive to capsaicin. It is known to be potent in activating vanilloid-1 receptor potential.This is believed to be the main receptor for nociception. It is also suggested to have capacity in the inhibition of NF-kB activation as a mechanism of action to generate the anti-inflammatory effect. The herb is often mixed with other natural anti-arthritic herbal preparations. It is also used for peripheral neuron disorders and chronic musculoskeletal pain (Caterina MJ; SurhYJ). Curcuma SPPSeveral members of the Curcuma genus are used in traditional medicine, the most important of which is Curcuma longa (CL); turmeric. Its rhizome has centuries-old use as a food spice and as a herb for its anti-inflammatory properties, hence its usefulness in arthritic conditions including rheumatoid arthritis (Sharma, 2006b). Animal studies. In an animal arthritis model, an essential oil-free CL preparation strongly suppressed joint inflammation and periarticular damage in correlation with reduced NF-kB activation and subsequent cascade of events (involving inflammatory mediators and of damage 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 bone appears to be comparable to that of betamethasone (Kamarudin, 2012). ; Taty Anna, 2011). overcome the problem of poor bioavailability generated by low water solubility. The osteoclast-osteoblast balance is unbalanced in favor of bone building, while stopping the progression of OA (Chang, 2015). arthritis induced in rats, applying ginger and turmeric). rhizomes were found to be better than indomethacin (a potent NSAID) in terms of their 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 diseases (Ramadan, 2013). In human clinical trials, a combination of Curcuma longa and Boswellia serrata has been shown to be more effective than a standard dose of celecoxib (a selective COX-2 inhibitor) in treating osteoarthritis, improving osteoarthritis conditions. patients, 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 an efficiency equivalent 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 in arthritis, but concluded that further studies are needed to definitively define it (Daily, 2016). Diferuloylmethane is the active ingredient of the phenolic pigment commonly known as curcumin, which carries out a complex beneficial action in various fields of pathology thanks to its ability to favorably influence a variety of signaling pathways and mediators (Ghosh, 2015). In a rat model of arthritis, it was shown to improve joint inflammation in the first few hours after the arthritis-inducing event, making it even more effective than a low dose of prednisone (Nonose, 2014).GarlicIt is well known that IL-1ß, once bound to its type 1 receptor, activates NF-?B dimers triggering the phosphorylation and subsequent degradation of inhibitory I?B proteins. NF-?B activation was a necessity for IL-1ß-induced MMP-13 secretion in OA chondrocytes (Kim SR, 2013. ) (Tsutsumi R., 2008. ). Furthermore, Imamura et al. demonstrated that IL-1ß and TNF-a inhibit chondrogenesis through the NF-?B pathway in human mesenchymal stem cells (Imamura M., 2014). Various garlic productshave been studied in osteoarthritis (Williams FMK, 2010). A sulfur compound isolated from garlic has been shown to suppress arthritis through inhibition of the DNA binding activity of NF-?B and the expression of iNOS and COX-2 (Ban JO, 2009.). However, there are some studies on the effect of SAMC on osteoarthritis. Furthermore, a previous study revealed that DATS suppressed the expression of MMP2-9 which depended on NF-?B and ERK-MAPK signaling pathways (Liu Y., 2015). Mechanistically, SAMC was found to correlate with increased IL-1ß-induced I?Ba levels, which subsequently mitigates p65 nuclear translocation and NF-?B transcriptional activity. Furthermore, our results indicated that IL-1ß treatment resulted in a significant increase in TNF-α expression at both mRNA and protein levels, which was enhanced by SAMC treatment. The combination of these findings suggests that SAMC can potentially be applied in the treatment of OA. GingerZingiber officinalis, also known as ginger, is a common spice used in Asian cuisine and a traditional remedy for joint diseases in ethnomedicine (Sharma, 2006a). Ginger is believed to have anti-inflammatory effects, possibly by inhibiting COX-1, COX-2, and LOX (Grzanna, 2005, ). However, pressed ginger extract paradoxically increased the synthesis of proinflammatory cytokines (TNF-α, IL-6, and monocyte chemotactic protein-1) in RAW264 cell culture (Ueda, 2010). Oral administration of ginger extract had a double effect on the synthesis of TNF-a in mice, in peritoneal cells: the ZO extract initially increased it, but with repeated administrations reduced it (Ueda, 2010 ). Furthermore, it increased the serum corticosterone level and this may contribute to the anti-inflammatory effect of ZO. A recent human clinical study found that ZO powder supplementation for three months can reduce the serum level of nitric oxide and high-sensitivity reactive protein hs-CRP in patients with knee OA. Inflammatory markers began to decrease after three weeks of treatment (Naderi, 2016). Several other studies have shown clinical improvement in OA patients with ZO extract assessed by VAS pain score, a reduction in the intake of rescue medications, mostly mild gastrointestinal adverse events, and a similar or similar efficacy and satisfaction score. even better than the standard treatment prescribed by the orthopedic specialist. The spicy-tasting ZO components were thought to contribute to the anti-inflammatory activity of this medicinal plant. For example, ginger inhibited kB kinase activity required for NF-kB activation and suppressed NF-kB-regulated expression of inflammatory genes in macrophages activated by lipopolysaccharide S (Lee, 2012). 6-dehydrogingerdione attenuated iNOS, COX-2, IL-1ß, IL-6, and TNF- gene expression, in vitro, in RAW 264.7 macrophages. (Huang, 2014,). Licorice About 300 polyphenols have been isolated from licorice, including phenolic acids, flavonoids, flavans, chalcones, isoflavan, and isoflavonoids. So far, the main active anti-inflammatory polyphenols found in licorice are chalcones, isoflavane and isoflavonoids. The mechanisms of the anti-inflammatory activities of chalcones have been thoroughly studied. LCA, LCB, ISL and EC all inhibited the production of NO, IL-6 and PGE2, while LCA, LCB and LCD all showed potent inhibition of lipid peroxidation (Fu Y, 2013. ) (Honda H, 2014. ) . LCB and LCD both strongly inhibited superoxide anion production in the xanthine oxidase system, showed potent DPPH radical scavenging activity, and inhibited NF-?B p65 phosphorylation (Furusawa J, 2009). Furthermore, LCC hasreduced 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-α, AKT, and p38 mitogen-activated protein kinase (MAPK). and attenuated degradation of I?Ba and NF-?B activity, as well as transcriptional activity of the activator protein AP-1 (Cho YC, 2010 ) (Lee HN, 2013. ). In addition to chalcones, other flavonoids contained in licorice, including DGC, DGD, ISOA, GLD, LID and LIA, have also shown excellent anti-inflammatory activities. DGC, DGD, and ISOA all showed strong iron-reducing activities and effectively scavenged DPPH, ABTS+, and singlet oxygen radicals (Kim HJ, 2012. ). Furthermore, DGC increased the expression of hemeoxygenase-1 and MAPK phosphatase-1, suppressed inflammation-mediated neurodegeneration, production of TNF-α, NO, ROS, NF-?B, and p38 phosphorylation. MAPK, ERK1/2, I?Ba and p65 (Kim J, 2013. ). GLD significantly inhibited the release of NO and IL-1ß (Thiyagarajan P, 2011. ), attenuated colonic inflammation in mice with dextran sulfate sodium-induced colitis, and reduced iNOS mRNA expression to elevated glucose levels, which indicated 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. ). PomegranateAs previously mentioned, in vivo studies have defined a clear role for NF-kB in the modulation of inflammation by pomegranate extracts, a result that appears 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, HS; Park, EK; genes, including IL-6 and interleukin 8 (IL-8), following exposure to proinflammatory 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 the inactivation of NF-kB signaling derived from pomegranate 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 a strong evidence base suggesting that pomegranate extract exerts anti-inflammatory effects that may relieve IBD symptoms (H.B. Kim, N.; Ivanov, I.; Pfent, CM; Prudhomme, KR; Bisson, W.H. Dashwood, RH; Talcott, ST; Mertens-Talcott, SU, 2016, ) and inflammation [23] were all improved by pomegranate fruit supplementation in rodent models of IBD. The mechanisms involved appear to be related to the inhibition of NF-_B (MAS- H. Rosillo, M.; Aparicio-Soto, M.; Sánchez-Fidalgo, S.; terminal kinase (JNK), extracellular signal-regulated kinase and transducer signal and activator of transcription phosphorylation 3 (MAS-H. Rosillo, M.; Cárdeno, A.; de la Lastra, CA, 2011, ).ResveratrolResveratrol has a variety of concentrations in different plants and it is believed that the concentrations higher ones derive from Knot weed or Polygonum cuspidatum and from red wine grapes.