Mechanisms of catalpol regulation of RASF against RA via MAPK/GBP5 signaling pathway

Volume 7, Issue 2, April 2022     |     PP. 56-65      |     PDF (477 K)    |     Pub. Date: May 14, 2022
DOI: 10.54647/biology18219    69 Downloads     5391 Views  

Author(s)

Mei Jie, Shandong Police General Hospital, China
He Qiang, Nanjing Hospital of Traditional Chinese Medicine, affiliated with Nanjing University of Traditional Chinese Medicine, China
Zhang Dapeng, Nanjing Hospital of Traditional Chinese Medicine, affiliated with Nanjing University of Traditional Chinese Medicine, China
Sun Xin, Nanjing Hospital of Traditional Chinese Medicine, affiliated with Nanjing University of Traditional Chinese Medicine, China

Abstract
Objective: Synovial fibroblasts (RASF) in rheumatoid arthritis are important mediators of synovial inflammation and joint destruction. This study provides valuable suggestions for the prevention and treatment of RA by observing catalase intervention in RASF and exploring its possible mechanisms.
Methods: An in vitro model of interleukin (IL)-1β-induced inflammatory synovial fibroblasts was established, and cells were intervened with different concentrations of catalpol (0, 20, 40, 60, 80, 100, 120, 140 μmol/L) for 6 h. Cell activity was measured by the CCK8 method; cells were divided into a blank group, a model group, a low dose of catalpol (20 μmol/L) group, a high dose of catalpol (100 μmol/L) group, and a high dose of catalpol (100 μmol/L) group. （The cells were divided into blank group, model group, catalpol low dose group (20 μmol/L), catalpol high dose group (100 μmol/L) and positive control group (methotrexate 100 nmol/L), and treated with different concentrations of catalpol (0 μmol/L, 20 μmol/L, 100 μmol/L) and methotrexate (100 nmol/L) for 2 h. The cells were then stimulated with IL-1β (20 ng) for 6 h. The cell supernatants were assayed by enzyme-linked immunosorbent assay (ELISA). The cell supernatant TNF-α, IL-6 and IL-17 contents were measured by ELISA kit; the protein expression levels of p-p38/p38, p-ERK/ERK, p-JNK/JNK and GBP5 in the cells were detected by protein immunoblotting (Western blotting).
Result: Compared with the blank group, the levels of TNF-α, IL-6, IL-17 and the protein expression of p-p38/p38, p-ERK/ERK, p-JNK/JNK, GBP5 were increased in the model group cells (P < 0.05); compared with the model group, the catalase low and high groups (concentrations of 20 μmol/L and 100 μmol/L, respectively) and the positive control Cells (methotrexate 100 nmol/L) showed decreased TNF-α, IL-6, IL-17 content and protein expression of p-p38/p38, p-ERK/ERK, p-JNK/JNK, GBP5 (P < 0.05). Compared with the blank group, the cell activities of the model group, catalpol low dose group (10 μmol/L) and positive control group were decreased, while the catalpol high dose group (100 μmol/L) had increased cell activities.
Conclusion: The results of in vitro cellular assays suggest that catalpol can inhibit inflammatory RASF and may be related to the inhibition of MAPK/GBP5 signaling-mediated pro-inflammatory cytokine release, and that catalpol has potential therapeutic value in RA.

Keywords
Catalponol; rheumatoid arthritis; synovial fibroblasts

Cite this paper
Mei Jie, He Qiang, Zhang Dapeng, Sun Xin, Mechanisms of catalpol regulation of RASF against RA via MAPK/GBP5 signaling pathway , SCIREA Journal of Biology. Volume 7, Issue 2, April 2022 | PP. 56-65. 10.54647/biology18219

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