Aloperine attenuates hydrogen peroxide-induced injury via anti-apoptotic activity and suppression of the nuclear factor-κB signaling pathway.

Aloperine is an alkaloid that exerts significant inhibitive effects on acute inflammation and Type III and IV hypersensitivity caused by a variety of inflammatory agents. The aims of the present study were to investigate whether the protective effect of aloperine attenuates hydrogen peroxide (HO)-induced injury, and to identify the underlying mechanisms involved. Nucleus pulposus cells were extracted from adult male Sprague-Dawley rats, and incubated with fresh medium containing 200 µM HO for 24 h. In the study, treatment with aloperine significantly increased cell viability and suppressed apoptosis in HO-treated nucleus pulposus cells in a dose-dependent manner. In addition, 10 and 100 nM aloperine significantly inhibited HO-induced tumor necrosis factor-α and interleukin-6 activities, and significantly increased the HO-reduced superoxide dismutase and glutathione peroxidase activities in nucleus pulposus cells (all P<0.01). However, aloperine treatment (10 and 100 nM) significantly reduced the HO-induced caspase-9 activity in nucleus pulposus cells. Furthermore, addition of 10 and 100 nM aloperine significantly suppressed nuclear factor-κB (NF-κB) and phosphorylated-protein kinase B expression levels in HO-treated nucleus pulposus cells. In conclusion, the protective effect of aloperine attenuated HO-induced injury via hyperproliferation, its anti-apoptotic activity and suppression of the NF-κB signaling pathway.