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

Ren,Dongliang; Ma,Weisong; Guo,Baozhen; Wang,Shunyi

doi:10.3892/etm.2016.3962

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

Authors:
- Dongliang Ren
- Weisong Ma
- Baozhen Guo
- Shunyi Wang
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Affiliations: Department of Orthopedics, The First Central Hospital of Baoding, Baoding, Hebei 071000, P.R. China
Published online on: December 7, 2016 https://doi.org/10.3892/etm.2016.3962
Pages: 315-320

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Abstract

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 (H2O2)‑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 H2O2 for 24 h. In the study, treatment with aloperine significantly increased cell viability and suppressed apoptosis in H2O2‑treated nucleus pulposus cells in a dose‑dependent manner. In addition, 10 and 100 nM aloperine significantly inhibited H2O2‑induced tumor necrosis factor‑α and interleukin‑6 activities, and significantly increased the H2O2‑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 H2O2‑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 H2O2‑treated nucleus pulposus cells. In conclusion, the protective effect of aloperine attenuated H2O2‑induced injury via hyperproliferation, its anti‑apoptotic activity and suppression of the NF‑κB signaling pathway.

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