Effects of Pingxian Particle on Cell Apoptosis of Hippocampal Neurons and Its Gene Expression in Epileptic Rat Model

Objective To investigate the molecular biological mechanism of Pingxian Particle's anti-epileptic effects on hippocampus neurons apoptosis.Methods Sixty Wistar rats were randomly assigned to normal control group,model group,positive control group,Pingxian large dose group and Pingxian small dose group.Except the normal control group,all the groups were intraperitoneally injected with 35 mg/kg pentylenetetrazol to induce epilepsy model.Pingxian large dose(1.66 g/mL) and small dose(0.42 g/mL) groups were intragastrically infused with Pingxian Particle 2 mL/d,the positive control group received 3.6 mg/mL phenobarbital suspension,the normal control group and model group were drenched with distilled water 2 mL/d for 5 weeks.The pathological changes of hippocampal neurons were observed dynamically by HE staining.The bcl-2 and bax protein positive cells were labeled with immunohistochemical SABC to dynamically observe the protein expression.Results The seizures of model group became more and more serious with kindle times,and the rats appeared grade Ⅰ-Ⅵ behavior during 1st-4th week.The onset times and onset grade of treatment groups were fewer and lower,and the highest grade were only Ⅳ,there were no significant differences in the onset grade and times between every two groups.The pathology represents of hippocampal neurons of treatment groups improved obviously.At the end of 3rd and 5th week,the number of bcl-2 protein expression at hippocampus in the model group was obviously less than the normal control group(P0.01),and that of Pingxian groups and positive control group were obviously more than the model group(P0.01).The number of bax protein expression at hippocampus in the model group was obviously more than the normal control group(P0.01),and that of Pingxian groups and positive control group were obviously less than the model group(P0.01).Conclusion Pingxian Particle may treat epilepsy though promoting the expression of bcl-2 and restraining the expression of bax.