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Published on: July 6, 2022
Scutellarin regulates osteoarthritis in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway
Shao-Hua Ju1, Li-Rong Tan2, Pan-Wang Liu3
1Department of Pharmacy, Sport Hospital Attached of CDSU, Chengdu Sport University, Chengdu, Sichuan 610041, P.R. China.
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 Erigeron breviscapus, 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 in vitro. 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 collagen II and SRY-box 9, whereas it suppressed the expression of matrix metalloproteinase 13. In addition, scutellarin downregulated the expression levels of cholesterol 25-hydroxylase and cytochrome P450 family 7 subfamily B polypeptide 1, but upregulated the expression of apolipoprotein A-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 in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway.
Insights
Scutellarin treatment in osteoarthritis cells reduced inflammatory markers and cholesterol-related proteins. This natural compound also inhibited the PI3K/AKT/mTOR pathway, suggesting therapeutic potential for osteoarthritis.
Area of Science:
- Biochemistry
- Pharmacology
- Cell Biology
Background:
- Osteoarthritis (OA) is a prevalent degenerative joint disease causing disability.
- OA involves cartilage destruction, inflammation, and cholesterol metabolism disruption.
- Scutellarin, from *Erigeron breviscapus*, has shown pharmacological benefits, but its OA effects are complex.
Purpose of the Study:
- To investigate scutellarin's effects on inflammatory cytokines in an OA cell model.
- To examine scutellarin's impact on collagen and cholesterol metabolism proteins.
- To determine if scutellarin regulates the PI3K/AKT/mTOR signaling pathway in OA cells.
Main Methods:
- An in vitro OA cell model was established using SW1353 cells stimulated with Interleukin-1β (IL-1β).
- Enzyme-linked immunosorbent assay (ELISA) and western blotting were employed to analyze protein expression.
- Effects of scutellarin on specific molecular markers and signaling pathways were assessed.
Main Results:
- Scutellarin increased collagen II and SOX9, while decreasing MMP-13 expression.
- It modulated cholesterol metabolism by downregulating CH25H and CYP7B1, and upregulating ApoA-1 and ABCA1.
- Scutellarin reduced IL-6 but not CRP or TNF-α, and inhibited the PI3K/AKT/mTOR pathway.
Conclusions:
- Scutellarin demonstrates multifaceted effects on key OA pathological pathways in vitro.
- It positively influences cartilage matrix proteins and cholesterol metabolism.
- Inhibition of the PI3K/AKT/mTOR pathway by scutellarin offers a potential therapeutic mechanism for OA.
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