Scoparone protects neuronal cells from oxygen glucose deprivation/reoxygenation injury.

Ischemic stroke is one of the leading causes of death and disability in the world. The cerebral ischemia/reperfusion (I/R) injury is considered as the major molecular mechanism in the pathogenesis of ischemic stroke. Scoparone, a major constituent of , has been found to exhibit protective effects against I/R-induced myocardial injury. However, the role of scoparone in cerebral I/R injury has not been elucidated. In the current study, the hippocampal neurons were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to simulate I/R injury . The results showed that scoparone improved OGD/R-induced inhibitory effect on cell viability of hippocampal neurons. Scoparone displayed anti-oxidative activity as proved by the decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in OGD/R-induced hippocampal neurons. In addition, cell apoptosis was markedly decreased after scoparone treatment in OGD/R-induced hippocampal neurons. The expression of bax was significantly decreased, while bcl-2 expression was increased in the scoparone pretreated hippocampal neurons. Furthermore, the expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were obviously induced by scoparone. Knockdown of Nrf2 by siRNA transfection dramatically attenuated the protective effects of scoparone on OGD/R-induced hippocampal neurons. Collectively, scoparone protected hippocampal neurons from OGD/R-induced injury activating Nrf2/HO-1 signaling pathway, suggesting that scoparone might be a potential agent for the ischemic stroke therapy.