The protective effect of butyphthalide on the cerebral ischemia-reperfusion injury of rats and the related molecular mechanism

摘要

Objective: To study the protective effect of butyphthalide on the cerebral ischemia-reperfusioninjury in rats and the related molecular mechanism. Methods: Male SD rats were selectedas the experimental animals and randomly divided into Sham group, ischemia-reperfusiongroup (I/R group) and butyphthalide group (NBP group), the ischemia-reperfusion modelswere established by suture method and then received 6 mg/kg butyphthalide sodium chlorideinjection before reperfusion for intervention. 12, 18 and 24 h after reperfusion, the number ofapoptotic cells in brain tissue as well as the levels of cell apoptosis molecules and oxidativestress molecules were determined. Results: 12, 18 and 24 h after reperfusion, analysis of thenumber of apoptotic cells in brain tissue of three groups of rats was as follows: the number ofapoptotic cells in brain tissue of I/R group was significantly more than that of Sham group (P＜0.05),and the Fas, FasL, BNIP3, Caspase-3 and Caspase-9 protein expression as well as reactiveoxygen species (ROS) and malondialdehyde (MDA) levels were significantly higher than thoseof Sham group (P＜0.05) while catalase (CAT) and superoxide dismutase (SOD) levels weresignificantly lower than those of Sham group (P＜0.05); the number of apoptotic cells in braintissue of NBP group was significantly less than that of I/R group, and the Fas, FasL, BNIP3,Caspase-3 and Caspase-9 protein expression as well as ROS and MDA levels were significantlylower than those of I/R group (P＜0.05) while CAT and SOD levels were significantly higherthan those of I/R group (P＜0.05). Conclusion: Butyphthalide can inhibit the apoptosis andoxidative stress reaction to reduce the cerebral ischemia-reperfusion injury in rats.