Galangin alleviates rheumatoid arthritis in rats by downregulating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease that greatly affect patients’ quality of life. Galangin extract is renowned for its anti-proliferative and anti-oxidative characteristics. However, galangin cytotoxicity studies are presently inadequate. We aimed to investigate the therapeutic potential of galangin on RA by investigating the PI3K/AKT signaling pathway.Fibroblast-like synovial cells (FLSs) were exposed to lipopolysaccharide (LPS) to establish an RA model in vitro . An ELISA assay was used to detect the levels of IL-1β, TNF-α, and IL-6. Cell viability and apoptosis were determined by CCK8/EdU and flow cytometry assays. A western blot assay was used to analyze the protein expression levels. An RA rat model was established to evaluate the function of galangin through histopathological examination. Our results found that galangin induced apoptosis, inhibited cell proliferation, and increased cell invasion of rheumatoid arthritis fibroblast-like synovial cells (RAFLSs). Galangin inactivated the PI3K/AKT signaling pathway and the inflammatory response. An agonist of PI3K signaling, 740Y‐P, restored the cellular functions of RAFLSs. Moreover, galangin suppressed the development of RA in vivo . Galangin effected its anti-arthritic influence through the PI3K/AKT signaling pathway. Galangin has potential as an alternative treatment for RA.

Galangin inhibits neointima formation induced by vascular injury via regulating the PI3K/AKT/mTOR pathway

“…8 In terms of mechanisms, galangin has reversed liver fibrosis by inhibiting the activation of the PI3K/AKT signaling pathway; 4 galangin has also alleviated rheumatoid arthritis by inhibiting the activation of the PI3K/AKT signaling pathway. 9 The PI3K/AKT signaling pathway plays an important role in the process of neointimal hyperplasia after vascular injury. 10,11 Therefore, it is speculated that galangin has potential regulatory effects on neointima hyperplasia.…”

Baicalein Induces Apoptosis of Rheumatoid Arthritis Synovial Fibroblasts through Inactivation of the PI3K/Akt/mTOR Pathway

“…Recent relevant studies reported that inactivation of the PI3K/Akt/mTOR signaling pathway enhanced autophagy, inhibited the proliferation and inflammatory response of synovial cells, and thus alleviated local symptoms of RA [ 39 ]. In addition, studies have also shown that galangin inhibited the development of RA through the PI3K/AKT signaling pathway, which also revealed a new mechanism which might be a feasible method for the treatment of RA [ 40 ]. Recent studies showed that BAI not only inhibited nasopharyngeal carcinoma (NPC) cells proliferation and induced NPC cells apoptosis but also blocked the PI3K/AKT and p53 signaling pathways in CNE2 cells [ 41 ].…”

The molecular mechanisms underlying anti‐inflammatory effects of galangin in different diseases

“…GAL caused apoptosis in FLSs, reduced cell growth, and promoted cell invasion. GAL inhibited the inflammatory response by lowering IL‐1β, TNF‐α, and IL‐6 levels and suppressing PI3K/AKT signal (X. Deng et al, 2022). Therefore, GAL may be a promising therapy for RA in the future.…”