OBJECTIVETo observe the effect of Pingxian granules on the protein expression of apoptosis regulatory genes Bcl-2 and Bax in the hippocampus of epileptic model rats and study the molecular biological mechanism of the anti-epileptic effect of Pingxian granules.

METHODTotally 60 45-days-old Wistar rats were selected and then randomly assigned into 5 groups: the normal control group, the model group, the positive control group, the Pingxian high dose group and the Pingxian low dose group, with 12 in each group. Except the normal control group, all the groups were intraperitoneally injected with 35 mg x kg(-1) pentylenetetrazol to establish the models of epilepsy. The Pingxian high dose (1.66 g x mL(-1)) and low dose (0.42 g x mL(-1)) groups were intragastrically infused with Pingxian granules 2 mL x d(-1). The positive control group received 3.6 g x L(-1) phenobarbital suspension by gastric perfusion. The normal group and the model group were drenched with distilled water, 2 mL x d(-1), for 5 weeks. Bcl-2 and Bax protein positive cells were labeled with immunohistochemical SABC at 3, 5 w.

RESULT(1) Rats in the model group appeared the epileptic behavior at the 1st week, and became serious with the kindle frequency; grade VIepileptic behavior appeared at the 4th week. The attack frequency and grade of the Pingxian group were less and lower, the highest grade were only IV, and there were no significant differences in the attack grade and frequency. (2) With the increase in kindle frequency, the model group showed a notable decrease in the Bcl-2 expression compared with the normal control group at the 3rd and 5th weekend (P < 0.01), but a significant increase in Bax protein expression (P <0. 01). The number of the Bcl-2 protein expression in Pingxian groups and the positive control group were obviously more than the model group (P < 0.01); and the number of the Bax protein expression in Pingxian groups and the positive control group were obviously less than the model group (P < 0.01).

CONCLUSIONPingxian granules may decrease neuronal cell apoptosis by improving the protein expression of apoptosis regulatory gene Bcl-2 and inhibiting the protein expression of apoptosis regulatory gene Bax with a view of anti-epilepsy.