Prx II reduces oxidative stress and cell senescence in chondrocytes by activating the p16-CDK4/6-pRb-E2F signaling pathway.

Abstract

Osteoarthritis (OA) is a common clinical degenerative disease and has a high incidence in the elderly. The purpose of this study was to explore the anti-oxidative stress and anti-aging effects of Peroxiredoxin II (Prx II) on articular chondrocytes, as well as its molecular mechanism. Articular cartilage tissues and culture human articular chondrocytes were selected. By constructing Prx II overexpressing lentivirus, the effects of Prx II on oxidative stress and cell senescence in chondrocytes were studied. Besides, the p16 overexpression lentivirus was constructed to investigate the effect of Prx II on the p16-CDK4/6-pRb-E2F signaling pathway (p16 signaling pathway). Articular cartilage tissues in patients with OA and IL-1β-induced chondrocytes expressed lower Prx II and had higher p16 signaling pathway activity. The overexpression of Prx II significantly increased the expression of SOD1 and SOD2 and decreased the expression of β-gal and P53/P21, indicating that Prx II can reduce the oxidative stress and senescence level of chondrocytes. Moreover, the overexpression of Prx II increased the expression of p16 signaling pathway-related molecules and the activation of the p16 signaling pathway attenuated the anti-oxidative stress and anti-aging effects of Prx II. Prx II can inhibit the p16 signaling pathway in chondrocytes to reduce the level of aging in chondrocytes, thereby reducing the level of oxidative stress in chondrocytes, and ultimately inhibiting the progression of OA.