| Objective To investigate the effects of miR-214-3p on chondrocyte autophagy and apoptosis induced by IL-1β and its possible mechanism. Methods Rat articular chondrocytes were induced by 10 ng/mL IL-1β for 24 h, to establish osteoarthritis (OA) cell model. The cells were divided into control group, model group, miR-NC group, miR-214-3p mimics group, 740Y-P (PI3K/AKT pathway activator) +miR-214-3p mimics group, and LY294002 (PI3K/AKT pathway inhibitor) +miR-214-3p mimics group. Cell viability was detected with CCK8. Cell apoptosis was detected with flow cytometry. Autophagosomes in cells were observed using transmission electron microscopy. Expressions of apoptosis (Bcl-2, Bax), autophagy (LC3II, Beclin-1), and PI3K/AKT pathway (AKT, p-AKT) related proteins were detected using Western blotting. Results Compared to those in the control group, the cell viability in the model group decreased (P<0.01), the apoptosis rate increased (P<0.01), autophagosomes decreased, the expression levels of Bcl-2, LC3II, and Beclin-1 proteins decreased (P<0.01), and Bax and p-AKT/AKT levels increased (P<0.01). Compared to those in the miR-NC group, cell viability in miR-214-3p mimics group increased (P<0.01), the apoptosis rate decreased (P<0.01), autophagosomes increased, the expression levels of Bcl-2, LC3II and Beclin-1 proteins increased (P<0.01), and Bax and p-AKT/AKT levels decreased (P<0.01). Compared to those in the effects of miR-214-3p mimics alone, the combination of 740Y-P reversed the above effects of miR-214-3p mimics, while the combination of LY294002 further aggravated the above effects of miR-214-3p mimics. Conclusion miR-214-3p promotes OA cell proliferation and autophagy, and inhibits apoptosis, which may be related to the inhibition of the activation of PI3K/AKT pathway. |