ABSTRACT
To investigate the protective effects of oxymatrine (OMT) against H2O2-induced damage in L02 cells and research the mechanism,L02 cells were used as the research object. The oxidative stress model of L02 was established by hydrogen peroxide (H2O2). CCK-8 was used to detect the cell activation of L02 cells treated by different OMT. FCM (flow cytometry) assay was used to evaluate the cell proliferation of L02 cells treated by OMT. The apoptosis of L02 cells was detected using Annexin-V/7-AAD apoptosis detection kit. The level of ROS was detected by DCFH-DA fluorescence probe. The GSH-PX and SOD were detected by micro plate and colorimetric method. Results showed that when the concentration of OMT is between 6.25 and 100 mg•L⁻¹, it could promote the production of NADPH and strengthen the activity of GSH-PX and SOD to get rid of the ROS to protect the L02 cell from the apoptosis of L02 cell induced by H2O2.
ABSTRACT
AIM:To observe the neuroprotection effects exogenous adrenomedullin(AM) against hypoxic-ischemia reperfusion damage(HIRBD) in neonatal rat models.METHODS:Forty neonatal rats were randomly divided into Control Group(n=8,with sham operation),Hypoxic-ischemia Reperfusion(HIR) Group and Intervention Group(n=8,wth intraperitoneal AM injection 0,6 and 12 h after making model).All rats were decapitated at 48 hours after reperfusion,and the cerebral slices were made at the 2 mm level in front of the interaural line.The pathobiological changes of brain tissue were observed by the method of HE dye in light microscope,and the levels of nitrogen monoxide synthase(NOS),glutathion(GSH) and myeloperoxidase(MPO) in neonatal rats cerebral tissue were determined by using chromatometry.RESULTS:Hypoxic-ischemia reperfusion could induce obviously cerebral pathological change which could be improved by AM.The brain tissue levels of cNOS and GSH in AM 0 and 6 h Group were significantly higher than those of HIR Group(P