Objective To investigate the protective mechanism of vinpocetine in brain injury traumatic(TBI)of rats.Methods250 Wistar rats were randomly divided into 5 groups:sham operation group,model group(intraperitoneal injection of normal saline)and vinpocetine group (intraperitoneal injection of 10mg/kg,20mg/kg and 40mg/kg),50 for each. The rats in the sham operation group only cranial skin incision,model group and vinpocetine group rats with Feeney free fall impact equipment caused by traumatic brain injury model,the administration of third days, seventh days and fourteenth days,the 5 groups were detected in rat plasma MDA(malondialdehyde)content and the activity of SOD,GSHx,CAT. On the fourteenth day,Western Blot was used to detect the expression of apoptosis protein Bcl-2,Bax,Caspase 3 and brain water in the brain tissue of 5 groups of rats.ResultsCompared with the model group,vinpocetine group(20mg/kg and 40mg/kg)of brain water content was significantly reduced(P all<0.05),plasma MDA decreased significantly(P<0.05,P<0.01);SOD,GSHx,CAT activity increased significantly(P<0.05, P<0.01);Bcl-2 increased significantly(P<0.05,P<0.01);Bax was significantly decreased(P<0.05,P<0.01);Caspase3 was significantly decreased(P<0.05,P<0.01).ConclusionVinpocetine can protect the brain injury through enhancing the antioxidant capacity,inhibiting the apoptosis pathway and relieving cerebral edema.%目的 探讨长春西汀对大鼠颅脑损伤(TBI)的保护机制.方法 250只Wistar大鼠随机分为5组:假手术组、模型组(腹腔注射生理盐水)和长春西汀组(腹腔注射10mg/kg、20mg/kg和40mg/kg),每组各50只.假手术组大鼠只进行颅部皮肤切口,模型组和长春西汀组大鼠采用Feeney自由落体撞击设备造成TBI模型,在给药的第3、7和14天,分别检测5组大鼠血浆中丙二醛(MDA)的含量以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、过氧化氢酶(CAT)的活性.第14天,Western Blot检测5组大鼠脑组织Bcl-2、Bax和Caspase3的表达,以及脑含水量.结果 与模型组比较,长春西汀组(20mg/kg和40mg/kg)脑含水量显著减少(P均<0.05),血浆MDA显著减少(P<0.05,P<0.01),SOD、GSHx、CAT活性显著增加(P<0.05,P<0.01),Bcl-2显著增加(P<0.05,P<0.01),Bax显著下降(P<0.05,P<0.01),Caspase 3表达显著下降(P<0.05,P<0.01).结论长春西汀能够通过提高抗氧化能力,抑制细胞凋亡通路,减轻脑水肿,对TBI起到保护作用.
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