Per2 attenuates LPS-induced chondrocyte injury through the PTEN/PI3K/Akt signalling pathway.

This research aimed to explore the role of period circadian clock 2 (Per2) in the evolution of osteoarthritis (OA) and the relevant mechanisms. Per2 messenger RNA (mRNA) and protein levels were markedly reduced in NHAC-kn cells treated with 5 µg/ml lipopolysaccharide (LPS) for 12 h. Then, pcDNA3.1-Per2 and si-Per2 were recruited to boost and reduce the expression of Per2, respectively. MTT assay, apoptosis analysis and enzyme-linked immunosorbent assay (ELISA) results showed that Per2 increased cell proliferation, while inhibited apoptosis and inflammation. Furthermore, the PTEN/PI3K/Akt signalling pathway was activated by Per2 overexpression; the CO-IP data confirmed that Per2 specifically bound to PTEN. Through employing IGF-1, a PI3K activator, we determined that Per2-mediated inflammation response in LPS-stimulated NHAC-kn cells through the PTEN/PI3K/Akt signalling pathway. In summary, the present study indicates that Per2 may serve as a novel therapeutic target through activating the PTEN/PI3K/Akt signalling pathway.