Effects of emodin on autophagy and cycle arrest in fibroblast-like synoviocytes in rheumatoid arthritis
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Hubei Minzu university Hubei Key Laboratory of Occurrence Intervention of Rheumatic Diseases

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    Abstract:

    Objective: Based on the cGAS/STING signaling pathway to investigate the potential effect of emodin (EMD) on autophagy of human rheumatoid arthritis fibroblast synovial cells (MH7A). Methods: CCK-8 method was used to detect the results of MH7A cell proliferation, and the concentration of drug was screened according to cell survival rate. Then, autophagy inhibitor 3-MA was added to further verify the effect of emodin on autophagy. Autophagy of MH7A cells was detected by MDC method. The protein expression levels of cGAS, STING, p-STING, LC3-I, LC3-II, p62 and Beclin-1 were detected by Western blot. Results: MDC staining indicated that emodin could enhance autophagy of MH7A cells. Western Blot results indicated that emodin could decrease the expressions of autophagy related proteins cGAS, STING, p-STING and P62, and increase the expressions of LC3-II and Beclin-1 in MH7A cells. After addition of autophagy inhibitor 3-MA, the expression of P62 protein in MH7A cells increased, while the expression of LC3-II and Beclin-1 protein decreased. Conclusion: Emodin may accelerate autophagy and inhibit MH7A cell proliferation by down-regulating cGAS/STING signaling pathway.

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History
  • Received:April 09,2023
  • Revised:September 13,2023
  • Adopted:January 05,2024
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