Eur J Med Res: Icariin alleviates osteoarthritis via the PI3K/Akt/mTOR/ULK1 signaling pathway

Objective: To investigate the effect of icariin (ICA) on interleukin-1β (IL-1β)-induced osteoarthritis (OA) and its possible mechanism
of action.

Methods: SW1353 chondrocytes were pretreated with ICA for 2h and then IL-1β
.
Matrix metalloproteinase (MMP-3) and type II collagen expression levels
were determined using real-time PCR and Western blot analysis.
Autophagy activation (via ICA) or inhibition (via shRNA)
is determined based on ULK1, Beclin-1, LC3-II/I, and p62 expression levels by Western blot analysis.
Phosphorylation levels
of PI3K, Akt, mTOR, and ULK1 were detected using Western blot analysis.

Results: IL-1β increased MMP-3 overproduction, induced type II collagen degradation, and decreased levels of autophagy-related proteins, including ULK1, Beclin-1, and LC3-II/I
.
In contrast, ICA pretreatment attenuated IL-1β-induced MMP-3 overproduction, increased the expression of type II collagen, and induced the expression
of autophagy-related proteins.
ICA also reduces PI3K, Akt, and mTOR phosphorylation, increases ULK1 production, and induces autophagy
.
shRNA-mediated ULK1 knockout leads to activation of the PI3K/Akt/mTOR pathway, thereby reversing the protective effects of
ICA.

Conclusion: ICA can induce autophagy
by regulating the PI3K/AKT/mTOR/ULK1 signaling pathway.
This study suggests that ICA may be effective in
treating OA.

Literature source:

Chen Y, Pan X, Zhao J, et al.
Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway.
Eur J Med Res.
2022; 27(1):204.
Published 2022 Oct 17.
doi:10.
1186/s40001-022-00820-x