Astragaloside IV relieves IL-1β-induced human nucleus pulposus cells degeneration through modulating PI3K/Akt signaling pathway.

Abstract

Intervertebral disc degeneration (IDD) is a multifactorial disease that is associated with nucleus pulposus (NP) apoptosis and extracellular matrix (ECM) degeneration and inflammation. Astragaloside IV (AS IV) has antioxidant, free radical scavenging, anti-inflammatory and anti-apoptosis effects. This study was to investigate whether AS IV could inhibit IL-1β-mediated apoptosis of HNP cells and its possible signal transduction pathway. Human nucleus pulposus cells (HNPCs) were stimulated with AS IV or LY294002 (PI3K inhibitor), followed by exposure to IL-1β for 24 hours. CCK8, TUNEL analysis and flow cytometry, ELISA and Western blotting were used to analyze the effects of AS IV on cell proliferation, apoptosis, inflammation, ECM and PI3K/Akt pathway signaling path-related proteins in IL-1β-induced HNPCs. Compared with IL-1β-induced HNPCs, AS IV could improve the proliferation activity and the expressions of Collagen II, Aggrecan and Bcl-2 proteins, inhibit the apoptosis rate, inflammation and Bax and cleaved caspase-3 protein expression, and increase the activity of PI3K/Akt pathway. LY294002 attenuated the protective effect of AS IV against IL-1β-induced HNPCs degeneration. AS IV can inhibit IL-1β-induced HNPCs apoptosis inflammation and ECM degeneration by activating PI3K/Akt signaling pathway, which can be an effective drug to reduce disc degeneration.