Schisandrin A alleviates chondrocyte senescence and extracellular matrix degeneration by suppressing PI3K/Akt signaling pathway.

Kecun Chen, Danqiu Xu, Yunrong Ding, Yanjun Cao, Huajun Bo

Department of Acupuncture and Massage, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, 1279 San Men Road, Shanghai 200434, China. · pubmed

Paper

Abstract

Osteoarthritis (OA) is a progressive joint disorder characterized by inflammation and metabolic imbalance. Schisandrin A (Sch-A), a bioactive compound from Schisandra sphenanthera, is known for its anti-inflammatory and protective properties. This study investigated the effects of Sch-A on chondrocyte senescence and metabolism using IL-1β-stimulated CHON-001 cells as an in vitro OA model. Sch-A showed no cytotoxicity up to 100 μM and alleviated IL-1β-induced chondrocyte injury. It restored anabolic metabolism, suppressed catabolic activity, and reduced inflammatory and fibrotic responses. Bioinformatics indicated links between Sch-A, cellular senescence, and the PI3K/Akt pathway. Functional assays confirmed that Sch-A suppressed senescence-associated secretory phenotype (SASP) factors, senescence markers, SA-β-galactosidase activity, and PI3K/Akt activation, while PI3K inhibition enhanced its anti-senescent effects. These findings suggest that Sch-A mitigates chondrocyte senescence and metabolic dysregulation by modulating PI3K/Akt signaling, supporting its therapeutic potential for OA.

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Research summary

Schisandrin A mitigates chondrocyte senescence and metabolic dysregulation by modulating the PI3K/Akt signaling pathway. The study addresses cellular senescence, a fundamental aspect of aging, and explores a potential therapeutic approach to counteract age-related degeneration in joint health.

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