Objective To investigate effects of antioxidant stress protein hem e oxygenase-1 (HO-1) on lipopolysaccharide (LPS)-induced endoplasm ic reticulum stress (ERS) of rat hepatocytes. Methods The BRL cells (rat hepatocyte cell line) were cultured. The hepatocytes were treated with LPS, LPS+HO-1 si RNA , HO-1 siRNA and PB S solution, respectively. The cell viability was m easured by trypan blue ex-clusion test. The apoptosis cells were detected by the fluorescent dye Hoechst 33258. E xpressions of GR P78, C HO P, caspase-12 and HO-1 were detected by Western blotting. Results LPS caused an in-crease of HO-1 protein expression of rat hepatocytes in a dose-dependent and tim e-dependent m anner, a up-regulation of GRP78, CHO P and caspase-12, a decrease in cellviability,and an increase in apopto-sis rate of hepatocytes. Pretreatm ent of HO-1 siRNA inhibited the up-regulation of LPS-induced HO-1, however, aggravated ERS and cellular injury. Conclusion HO-1 inhibites ERS-m ediated cellular injury of rat hepatocytes induced by LPS.

Objective:To study the neuro-protective effects of Shenfu injection on Nrf 2 signaling pathway affected by cerebral ischemia reperfusion.Methods: A total of 68 adult male Sprague-Dawley rats were randomly divided into sham group , cerebral ischemia-reperfusion group,and(8 mg/kg)Shenfu injection treatment group.Shenfu injection was injected intraperitoneally in the rats after MCAO.Neurologic deficit was evaluated after 24 hours of reperfusion.All the rats were sacrificed after 24 h of ischemia-reoerfusion for biochemical analysis or Nissl staining.Results:Shenfu injection treatment significantly increased the expression of Nrf 2,HO-1 and NQO-1(P<0.05).Furthermore,Shenfu injection treatment significantly reduced the expression of cleaved -caspase-3 and attenuated neurological deficits after cerebral ischemia reperfusion ( P<0.05 ).Lastly, Shenfu injection could evidently alleviate the severity of neuronal degeneration ( P<0.05 ).Conclusion:Shenfu injection could confer neuroprotection after cerebral ischemia reperfusion through modulating the Nrf2 signaling pathway.