Scutellarin regulates osteoarthritis in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

Abstract

Osteoarthritis(OA) is a highly prevalent disease worldwide that causes disability and diminishes the quality of life of affected individuals. The disease is characterized by cartilage destruction, increased inflammatory responses and cholesterol metabolic disorder. Scutellarin is the major active ingredient extracted from Erigeronbreviscapus, and it has been demonstrated to possess various pharmacological functions in the treatment of the disease. However, its effects on OA are complex. The present study investigated whether scutellarin can mediate the release of inflammatory cytokines, the expression of collagen- and cholesterol-related proteins, and regulate the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin(mTOR) signaling pathway in a cell model of OA. Interleukin(IL)-1β was used to stimulate OA in SW1353 cells invitro. The primary methods used were ELISA and western blotting, which were carried out to examine the effects of scutellarin on the cell model of OA. It was found that scutellarin increased the expression of collagenII and SRY-box 9, whereas it suppressed the expression of matrix metalloproteinase13. In addition, scutellarin downregulated the expression levels of cholesterol 25-hydroxylase and cytochrome P450 family7 subfamilyB polypeptide1, but upregulated the expression of apolipoproteinA-1 and adenosine triphosphate-binding cassette transporter A1. The IL-1β-induced increase in the expression of IL-6 was decreased by treatment with scutellarin; however, scutellarin did not alter the expression of C-reactive protein and tumor necrosis factor-α. The protein expression levels of AKT, phosphorylated (p)-AKT, mTOR and p-mTOR in the PI3K/AKT/mTOR signaling pathway were decreased in the IL-1β-induced SW1353 cells following scutellarin treatment. Overall, the findings of the present study demonstrated that scutellarin regulated OA invitro by inhibiting the PI3K/AKT/mTOR signaling pathway.