The Inhibition Role of ALDH2 Activated by Omeprazole on Apoptosis of Neuron

Objective To investigate the effects of omeprazole(OME) on injured neuron induced by oxygen glucose deprivation(OGD) and the possible mechanism.Methods A SD pregnant rats was selected,on day 15 ~ 16 of gestation,neurons isolated from newborn rat cerebral cortex were cultured in vitro for seven days,then neurons were randomly divided into control group,OGD group,and OGD + OME group(3,10,30,100,300 μg / ml OME was added in separately).Proliferation of neurons was detected by CCK-8.Injury and apoptosis of neurons were detected by Hoechst 33342 fluorescence staining and TUNEL,neurons apoptosis rate was detected by Annexin V / PI flow cytometry.To observe the effects of ALDH2 agonist(Adal1) and retardant(Cya) on injured neuron induced by OGD.Neurons of control group,OGD group and OGD + OME group(10 μg / ml OME) were collected,the activities of ALDH2 were measured.Results Proliferation of primary neurons which were cultured in vitro in OGD group was significantly lower than that in control group 〔OD450:(0.370 ±0.027) vs.(0.959 ±0.062),P 0.05〕.Apoptosis rate of primary neurons in OGD group was significantly higher than that in control group 〔(33.53 ± 1.41) % vs.(15.42 ± 1.29) %,P 0.05〕.Proliferation of primary neurons in OGD + OME group(10,30 μg / ml OME) was significantly higher than that in OGD group(P 0.05),apoptosis rate of primary neurons in OGD + OME group(10,30 μg / ml OME) was significantly lower than that in OGD group(P 0.05).Apoptosis rate of primary neurons in which ALDH2 agonist(Adal1) were added was significantly lower than that in OGD group 〔(16.73 ±0.62) %vs.(28.92 ±0.12) %,P 0.05〕.Apoptosis rate of primary neurons in which retardant(Cya) were added was significantly higher than that in OGD group 〔(45.22 ± 3.23) % vs.(28.92 ± 0.12) %,P 0.05〕.Compared with the control group,the activities of ALDH2 in neurons among OGD group decreased by 74.01%,OME(10 μg / ml) increased the activities of ALDH2 in neurons among OGD group by 130.00%.Conclusion OME can protect injured neuron induced by OGD,which may be related to anti-apoptosis and increasing the activity of ALDH2.