Astragaloside regulates lncRNA LOC100912373 and the miR‑17‑5p/PDK1 axis to inhibit the proliferation of fibroblast‑like synoviocytes in rats with rheumatoid arthritis.

Abstract

Previous studies have confirmed that astragaloside (AST) exerts a positive effect on alleviating synovial and joint injury in rheumatoid arthritis (RA). However, the precise mechanisms through which AST acts in the treatment of RA remain unclear. Long non-coding RNA (lncRNA) LOC100912373 was identified as a key gene related to RA and has been proven to interact with miR-17-5p, in order to regulate the pyruvate dehydrogenase kinase 1 and protein kinase B axis (PDK1/AKT axis). The present study aimed to determine whether AST may treat RA through the interaction between lncRNA LOC100912373 and the miR-17-5p/PDK1 axis. MTT assays and flow cytometry were used to detect the proliferation and cell cycle progression of AST-treated fibroblast-like synoviocytes (FLSs). The expression of lncRNA LOC100912373 and miR-17-5p, as well as relative the mRNA expression of the PDK1 and AKT genes following AST intervention was detected by reverse transcription-quantitative PCR (RT-qPCR), immunofluorescence and western blot analysis. The results revealed that AST inhibited FLS proliferation, reduced lncRNA LOC100912373 expression levels, increased miR-17-5p expression levels, and decreased the PDK1 and p-AKT expression levels. Additionally, consecutive rescue experiments revealed that AST counteracted the effects of lncRNA LOC100912373 overexpression on FLS proliferation and cell cycle progression. On the whole, the present study demonstrates that AST inhibits FLS proliferation by regulating the expression of lncRNA LOC100912373 and the miR-17-5p/PDK1 axis.