Icariin Prevents H2O2-Induced Apoptosis via the PI3KAkt Pathway in Rat Nucleus Pulposus Intervertebral Disc Cells

Abstract EN

Icariin is a prenylated flavonol glycoside derived from the Chinese herb Epimedium sagittatum.

This study investigated the mechanism by which icariin prevents H2O2-induced apoptosis in rat nucleus pulposus (NP) cells.

NP cells were isolated from the rat intervertebral disc and they were divided into five groups after 3 passages: (A) blank control; (B) 200 μM H2O2; (C) 200 μM H2O2 + 20 μM icariin; (D) 20 μM icariin + 200 μM H2O2 + 25 μM LY294002; (E) 200 μM H2O2 + 25 μM LY294002.

LY294002 is a selective inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway.

NP cell viability, apoptosis rate, intracellular reactive oxygen species levels, and the expression of AKT, p-AKT, p53, Bcl-2, Bax, caspase-3 were estimated.

The results show that, compared with the control group, H2O2 significantly increased NP cell apoptosis and the level of intracellular ROS.

Icariin pretreatment significantly decreased H2O2-induced apoptosis and intracellular ROS and upregulated p-Akt and BCL-2 and downregulated caspase-3 and Bax.

LY294002 abolished the protective effects of icariin.

Our results show that icariin can attenuate H2O2-induced apoptosis in rat nucleus pulposus cells and PI3K/AKT pathway is at least partly included in this protection effect.