Protective Effect Of Compound Acanthopanax Senticosus Injection On Cerebral Ischemia Reperfusion Injury In Rats And Its Mechanism

Obiective: To investigate protective effect of compound acanthopanaxsenticosus injection on Cerebral ischemia reperfusion injury in rats and itsmechanism.Method: Choose50male Wistar rats totally, provided by the laboratoryanimal center of jilin university. The rats were randomly divided into thesham operation, infarction model group, CASI25mg/kg，CASI50mg/kg，CASI100mg/kg groups and each group of10. Drug groups were givenIntraperitoneal injection for3days, once each day. Sham group andinfarction model group were given equal volumetric physiological saline.Reperfusion rat middle cerebral artery occlusion model was Prepared withZea longa improved line bolt. Nerve function defect score was inspect byKruskal-Wallis. The brain index and the brain water content were calculatedaccording to the formula. Ultrastructural pathological changes were observed.The whole blood viscosity and plasma viscosity were detected. The changesof PGI2, TXA2, SOD and MDA in the serum were measured. Using theSPSS statistical software13.0, quantitate data comparison between the twogroups with t test, P <0.05was statistically significant.Result：1．Compared with the sham group, the nerve symptom scoreswere decreased more obviously in the infarction model group, after cerebralischemia/reperfusion(P <0.001); Compared with the infarction model group,the nerve symptom scores in all three dose CASI groups were significantlyless (P <0.05or P <0.01).2．Compared with the sham group, the brain water content and the brainindex in model group were significantly increased (P <0.01or P <0.001). The brain water content in CASI50mg/kg，CASI100mg/kg groups weresignificantly less than model group (P <0.05or P <0.01), Compared withmodel group, the brain index in CASI three dose groups were significantlyless (P <0.01or P <0.001).3．The development of ultrastructral pathological changes in CASI threedose groups obviously improved compared with the infarction model group.4．Compared with the sham group, the whole blood viscosity at lowshear rate (10/s), middle shear rate(60/s), high shear rate(120/s) and plasmaviscosity in the infarction model group were significantly increased (P <0.05or P <0.01). Compared with infarction model group, the whole bloodviscosity at low shear rate and high shear rate in all CASI three dose groupswere significantly increased (P <0.05or P <0.01). CASI50mg/kg and CASI100mg/kg groups can also decrease the whole blood viscosity at middleshear rate and plasma viscosity (P <0.05).5．Compared with the sham group, the model group’s plasma TXA2level increased significantly, PGI2/TXA2ratio and PGI2level decreasedobviously (P <0.01or P <0.001). Compared with infarction model group,plasma TXA2level were significantly declined in CASI50mg/kg and CASI100mg/kg groups, plasma PGI2level and PG I2/TXA2ratio were enhanced(P <0.05, P <0.001).6．Compared with the sham group, the infarction model group’s serumMDA content increased, SOD activity decreased obviously (P <0.01or P < 0.001). Compared with the infarction model group, CASI three dose groupscan reduced serum MDA content, and increased SOD activity (P <0.05, P <0.05).Conclusion:1．CASI can improve the damaged nerve function, relievecerebral edema.2．CASI can resist thrombosis and platelet aggregation.3．CASI has protective effect on cerebral ischemia reperfusion injury byreducing oxidative damage of free radicals, it play an important role inprotecting brain cells.