[17β-estradiol inhibits interleukin-1β-induced rat nucleus pulposus cell apoptosis through the PI3K/Akt/mTOR signal pathway].

The apoptosis of nucleus pulposus cells (NPCs) is the main cellular process of intervertebral disc degeneration (IVDD). Our previous studies showed that 17β-estradiol (E) protects rat NPCs from interleukin-1β (IL-1β)-induced apoptosis via the PI3K/Akt signaling pathway. This study was aimed to investigate whether downstream proteins of PI3K/Akt pathway were involved in inhibition of E on NPCs' apoptosis. Primary culture of rat NPCs was isolated by trypsin digestion. Being pretreated with E and different inhibitors of downstream proteins of PI3K/Akt pathway, the NPCs were treated with IL-1β. Cellular apoptosis was detected by Annexin V/PI staining. Cell viability was detected by CCK-8. Cell adhesion was evaluated by cell-collagen binding assay. Phosphorylation levels of mammalian target of Rapamycin (mTOR), glycogen synthase kinase-3β (GSK-3β) and nuclear factor κB (NF-κB) were detected by Western blot. The results showed that E significantly inhibited the IL-1β-induced apoptosis of NPCs, reversed the decrease of cell viability and adhesion induced by IL-1β, and inhibited the down-regulation of mTOR phosphorylation level induced by IL-1β. Rapamycin could block these protective effects of E. These results suggest that E may inhibit IL-1β-induced NPCs' apoptosis through the PI3K/Akt/mTOR signaling pathway.