Study Of Effect Of Shenhuanghuakeli On Nerve Cell Apoptosis And Hemorheology In Rats With Focal Cerebral Ischemial/Reperfusion

Objective: To observe the effects of compound preparation of traditional Chinesemedicine called shenhuanghuakeli on nerve cell apoptosis and hemorheology in SD ratwith middle cerebral artery occlusion, and provide for the clinical prevention andtreatment of ischemic cerebrovascular disease with a drug of choice.Methods: The rats were randomly divided into sham operation group, model group andshenhuanghuakeli-low （0.2g/kg）, shenhuanghuakeli-middle （0.6g/kg）,shenhuanghuakeli-high（1.8g/kg）group, positive drug(vitamin E or aspirin) groupbefore molding operation, with continuous intragastric administration of7D, once aday, in which the sham operation group and model group were given the same amountof physiological saline. The rats were made by the occlusion of middle cerebral arterywith suture embolus, ischemia for30minutes and reperfusion for7days, with thesame administration. The amount of Bcl-2, Bax expression in ipsilateral cerebral cortexof rats in each group was detected by western blot, and observed byimmunohistochemical method. The activity of pro-apoptotic enzyme Cleaved caspase-3and Cleaved caspase-9in each rat ipsilateral striatum was determined byspectrophotometric measurement. The coagulation function, hematocrit, blood andplasma viscosity of rat blood in each group are measured according to the kit manuls.Results:1. Bcl-2and Bax gene expressions in ipsilateral cerebral cortex of model groupimbalanced, and Bcl-2/Bax ratio decreased. Bcl-2/Bax ratio of shenhuanghuakeli-highgroup were significantly higher than those in the model group (P <0.05).2. Bcl-2andBax gene mainly expressed in nerve cell cytoplasmic of ipsilateral brain.3. The activities of pro-apoptotic enzyme Cleaved caspase-3and Cleaved caspase-9ofipsilateral striatum in model group were significantly higher than those in shamoperation group (P <0.01). Compared with the model group, the enzyme activity ofeach shenhuanghuakeli group was significantly decreased (P <0.05), and presentscertain dose-effect relationship.4. Hematocrit, blood viscosity and plasma viscosity ofmodel group significantly increased (P <0.01). Compared with sham operation group,those in each shenhuanghuakeli group decreased significantly (P <0.05).5. Comparedwith model group, TT, PT and APTT of shenhuanghuakeli group were significantlyprolonged(P <0.05), but Fib had no difference.Conclusion:1.Shenhuanghuakeli can inhibit nerve cell apoptosis which induced byischemia reperfusion injury. The mechanism may be regulating apoptosis geneexpression, and reducing the activity of pro-apoptosis enzyme.2. Shenhuanghuakel canreduce blood viscosity which induced by ischemia reperfusion injury, and improveblood coagulation function.