Suppression of the onset and progression of collagen-induced arthritis in rats by QFGJS, a preparation from an anti-arthritic Chinese herbal formula

Cai, Xiong; Zhou, Hua; Wong, Yuen Fan; Xie, Ying; Liu, Zhong Qiu; Jiang, Zhi Hong; Bian, Zhao Xiang; Hong, Xu; Liu, Liang

doi:10.1016/j.jep.2006.09.008

Cited by 57 publications

(43 citation statements)

References 39 publications

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“…NF-κB is a ubiquitous transcription factor that plays a key role in the expression of many genes central to RA, including IL-1β in monocytes, as well as intercellular adhesion molecule-1 (ICAM-1), TNF-α and IL-6 [26][27][28]. The present study indicated that additional treatment with TCDCA reduced the elevated binding activity on a concentration-dependent manner ( Figure 6).…”

Section: Effects Of Tcdca On Expression Of Iκbα and Phospho-iκbαsupporting

confidence: 52%

Taurochenodeoxycholic Acid Suppresses NF-κB Activation and Related Cytokines Expression in Peritoneal Macrophages from Adjuvant Arthritis Rat

Mao¹,

Liu²,

Guan³

et al. 2018

Rec.Nat.Prod.

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Taurochenodeoxycholic acid (TCDCA) is one of main bioactive substances of animals' bile acid and confers good anti-inflammatory activity. This study aimed to investigate the mechanism of the anti-adjuvant arthritis activity of TCDCA, the actions were observed in vitro on the protein and mRNA expression of cytokines, the activity of nuclear factor-kappa B (NF-κB) and its inhibitory IκBα protein level of peritoneal macrophages (PMs) in adjuvant arthritis (AA) rats. In a definite concentration ranging from 150 μg/mL to 200 μg/mL, the over protein and mRNA expression of TNF-α, IL-1β and IL-6 were remarkably suppressed in the supernatant of PMs treatment with TCDCA. Positive correlations were found between changes of NF-κB activity and expression of TNF-α, IL-1β and IL-6 influenced by TCDCA. The activity of NF-κB was markedly inhibited and IκBα protein level was increased by TCDCA (150 μg/mL,180 μg/mL and 200 μg/mL). TCDCA suppresses the protein and mRNA expression of TNF-α, IL-1β, and IL-6 by inhibiting the NF-κB binding activity, which is mediated through up-regulating the IκBα expression of PMs in AA rats.

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Section: Effects Of Tcdca On Expression Of Iκbα and Phospho-iκbαsupporting

confidence: 52%

Taurochenodeoxycholic Acid Suppresses NF-κB Activation and Related Cytokines Expression in Peritoneal Macrophages from Adjuvant Arthritis Rat

Mao¹,

Liu²,

Guan³

et al. 2018

Rec.Nat.Prod.

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“…A variety of issues exist with DMARDs (35). The use of methotrexate and leflunomide is limited by their long-term side effects and toxicity (36,37). In this study, we compared the efficacy and mechanism of action of iguratimod, a novel DMARD, with those of classical DMARDs in CIA.…”

Section: Discussionmentioning

confidence: 99%

A Novel Disease-Modifying Antirheumatic Drug, Iguratimod, Ameliorates Murine Arthritis by Blocking IL-17 Signaling, Distinct from Methotrexate and Leflunomide

Luo

Sun

et al. 2013

The Journal of Immunology

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Iguratimod, a novel disease-modifying antirheumatic drug, which is now used in clinics in China and Japan, has been confirmed as a highly efficacious and safe drug for rheumatoid arthritis therapy. The antiarthritic mechanism of iguratimod, especially compared with that of the classical disease-modifying antirheumatic drugs, has not been elucidated. In this study, we conducted a comparative analysis of the antiarthritic effects of iguratimod and two reference drugs, methotrexate and leflunomide. We found that iguratimod dose dependently and potently inhibited arthritic inflammation of the synovium in collagen-induced arthritis and predominantly targeted IL-17 signaling. Consistent with its effects in vivo, iguratimod significantly suppressed the expression of various proinflammatory factors triggered by IL-17 in the cultured fibroblast-like synoviocytes. The inhibition of IL-17 signaling by iguratimod was further linked to a decrease in the mRNA stability of related genes and a reduction in phosphorylation of MAPKs. Iguratimod mainly targets Act1 to disrupt the interaction between Act1 and TRAF5 and IKKi in the IL-17 pathway of synoviocytes. Together, our results suggest that iguratimod yields a strong improvement in arthritis via its unique suppression of IL-17 signaling in fibroblast-like synoviocytes. This feature of iguratimod is different from those of methotrexate and leflunomide. This study may be helpful for further understanding the unique antiarthritic mechanism of iguratimod in patients with rheumatoid arthritis.

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“…The X-ray parameters were 40 kV, 100 mA, and 0.02 millisecond. Images were read independently in a blinded fashion, and radiologic score was assessed according to the following criteria: 0) no radiologic changes were observed; 1) mild changes, with tissue swelling and edema; 2) moderate changes, with joint erosion and disfiguration; and 3) severe changes, with bone erosion and osteophyte formation (Cai et al, 2007). The total radiologic scores were calculated from the sum of both hind paws of each rat; the maximum value was 6.…”

Section: Methodsmentioning

confidence: 99%

Inhibitory Effect of Baicalin on Collagen-Induced Arthritis in Rats through the Nuclear Factor–κB Pathway

Wang

Huang

et al. 2014

J Pharmacol Exp Ther

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This study focused on the potential therapeutic effect of baicalin on collagen-induced arthritis (CIA) in rats and the underlying mechanisms. The CIA rats were injected with baicalin (50, 100, or 200 mg/kg) once daily for 30 days. The rats were monitored for clinical severity of arthritis, and joint tissues were used for radiographic assessment and histologic examination. We quantified tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b) in experimental animals and used Western blots to assess levels of protein abundance, phosphorylation, and acetylation of nuclear factor (NF)-kB p65 and sirtuin 1 (sirt1) protein expression in joint tissues. Human fibroblast-like synoviocytes from rheumatoid arthritis (HFLS-RA) were adopted in further mechanistic investigations. Baicalin intraperitoneal injection for 30 days dose-dependently blocked clinical manifestations of CIA, such as functional impairment and swollen red paws. Meanwhile, it alleviated collageninduced joint inflammation injury and inhibited the secretion of TNF-a and IL-1b in both rat synovium and HFLS-RA. Further mechanistic investigations revealed that baicalin suppresses NF-kB p65 protein expression and phosphorylation in synovial tissue and human-derived synoviocytes. Moreover, the acetylation of NF-kB p65 was downregulated by baicalin, which negatively correlates with the baicalin-induced upregulation of sirt1 expression in the same conditions. The data indicate that CIA in rats can be alleviated by baicalin treatment via relieving joint inflammation, which is related to the suppression of synovial NF-kB p65 protein expression and the elevation of its deacetylation by sirt1.

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Suppression of the onset and progression of collagen-induced arthritis in rats by QFGJS, a preparation from an anti-arthritic Chinese herbal formula

Cited by 57 publications

References 39 publications

Taurochenodeoxycholic Acid Suppresses NF-κB Activation and Related Cytokines Expression in Peritoneal Macrophages from Adjuvant Arthritis Rat

Taurochenodeoxycholic Acid Suppresses NF-κB Activation and Related Cytokines Expression in Peritoneal Macrophages from Adjuvant Arthritis Rat

A Novel Disease-Modifying Antirheumatic Drug, Iguratimod, Ameliorates Murine Arthritis by Blocking IL-17 Signaling, Distinct from Methotrexate and Leflunomide

Inhibitory Effect of Baicalin on Collagen-Induced Arthritis in Rats through the Nuclear Factor–κB Pathway

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