Qinteng Tongbi Decoction Medicated Serum Exerts Regulates the Proliferation, Migration, and Apoptosis of Synovial Fibroblasts in Adjuvant-Induced Arthritis Rats Model via Phosphatidylinositol 3-Kinase/Protein Kinase B Signaling Pathway

Abstract

Background Qinteng Tongbi decoction (QTTBD) was an empirical prescription that could effectively prevent and treat rheumatoid arthritis (RA), but there was no report of pharmacological studies on this prescription. The purpose of this paper was to report the effects of QTTBD on the proliferation, migration, and apoptosis of synovial fibroblasts in adjuvant arthritis model rats, and to reveal its anti-RA regulatory mechanism. Methods To divide the fibroblast-like synovial (FLS) cells of experimental rats into 6 groups (blank control group, model control group, positive drug group, QTTBD high, medium, and low dose groups) and cultured with serum-containing drugs. And using Cell Counting Kit-8 to detect the proliferation rate of FLS cells, flow cytometry to detect the apoptosis of FLS cells, the enzyme-linked immunosorbent assay method to detect the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α), Western Blot to detect phosphatidylinositol 3-kinase (PI3K), AKT1, p-AKT1, Bax and Bcl-2 gene and protein expression. Results Experimental results showed that QTTBD-containing serum could effectively inhibit the proliferation of FLS cells ( p <0 .05), induce the apoptosis of FLS cells, reduce the expression levels of inflammatory factors such as IL-6, IL-1β, and TNF-α ( p <0 .05), reduce expression of PI3K, AKT1, p-AKT1, and Bax ( p <0 .05), while the Bcl-2 expression increased ( p <0 .05). Conclusion QTTBD could effectively regulate the proliferation, migration, and apoptosis of FLS cells in adjuvant-induced arthritis (AIA) rats, and its mechanism might be related to regulating the level of inflammatory factors and intervening in the PI3K/protein kinase B (AKT) signaling pathway.