Emodin anti-oxidative stress damage of rat cortical neurons induced by Aβ_(25~35)

Objective To investigate the mechanisms of emodin against Aβ25~35-inducing oxidative stress-triggered damage in primary culture of rat cortical neurons. Methods Primary cultured rat cortical neurons were randomly divided into 5 groups:control,model,3 doses of emodin groups treated with different concentrations. The activities of superoxide dismutase( SOD) and glutathione peroxidase( GSHPx) and the content of malondialdehyde( MDA) were assayed by colorimetric assay. To study the change of reactive oxygen species( ROS) content in cortical neurons,the DCF fluorescence intensity of H2DCF-DA-stained cells was observed by fluorescence microscope and detected by FCM. The change of mitochondrial membrane potential( △Ψm),the rhodamine123( Rh123) fluorescence intensity of cortical neurons with Rh123 stain was detected by FCM. Release of cytochrome C from mitochondrial membrane was determined by Western blot analysis. Results Exposure of cortical neurons to 30 μmol /L Aβ 25 ~ 35 decreased activities of SOD and GSH-Px as well as increased levels of MDA production. In parallel,Aβ 25 ~ 35 significant increased the intracellular ROS elevation and decreased the level of △Ψm. However,pretreatment of the cells with emodin prior to Aβ 25 ~ 35 exposure suppressed these Aβ 25 ~ 35-induced cellular events noticeably. In addition,emodin reduced the level of cytochrome C. Conclusions The emodin prevents Aβ 25 ~ 35-induced cell damage in primarily cultured cortical neurons by rescuing loss of antioxidant enzyme activities and decreasing the level of △Ψm and inhibiting an increase in MDA,ROS and cytochrome C.