维奥欣对脑缺血再灌注损伤大鼠的脑保护作用

目的:探讨维奥欣对脑缺血再灌注损伤(CIRI)大鼠的脑保护作用及可能的作用机制。方法:70只Wistar大鼠随机分为假手术对照组10只、CIRI组30只和维奥欣组30只,测定再灌注30,60和120min时血清及肺组织一氧化氮(NO)、丙二醛(MDA)浓度、超氧化物歧化酶(SOD)和Na~+-K~+-ATP酶活性,观察脑超微结构的变化。结果:脑缺血再灌注期间,CIRI组血清和脑组织中SOD活性、脑组织中Na~+-K~+-AFP酶活性与假手术对照组比较明显下降(P<0.01和P<0.05);NO和MDA浓度显著升高(P<0.01和P<0.05);脑超微结构发生异常改变,维奥欣组上述各指标的异常变化与CIRI组相比明显减轻(P<0.01)。结论:维奥欣对CIRI具有良好的保护作用,其机制可能与提高机体SOD和Na~+-K~+-ATP酶活性、降低NO水平和MDA浓度及减轻氧自由基损伤等有关。

Effect of Viocin in protection of cerebral ischemic reperfusion injury in rats

Objective: To evaluate the effectiveness of Viocin in the protection of cerebral ischemic reperfusion injury (CIRI) in rats. Methods:70 Wistar rats were randomly divided into three groups:sham operation control(n = 10), CIRI induction(n = 30) and Viocin pretreatment(n =30) followed by CIRI induction. The following parameters post the induction of CIRI for 30, 60 and 120minutes were measured in serum and cerebral tissues:levels of nitric oxide (NO) and malondialdehyde (MDA). activities of superoxide dismutase(SOD) and Na~+ -K~+ -ATP synthase, and changes of cerebral ultra-microstructure. Results: Compared to the sham operation group, CIRI group significantly decreased the activities of SOD (P<0.01 ) and Na~+ -K~+ -ATP synthase (P<0.05), and increased the levels of NO (P<0.01) and MDA (P<0.05). The cerebral ultra-microstructure was deformed in CIRI. The changed of corresponding parameters in Viocin group was not so remarkable as the ones in CIRI group(P<0.01 ). Conclusion: Significant protection on the CIRI was evident in Viocin-pretreated rats,which achieved by increasing the activities of SOD and Na~+ -K~+ -ATP synthase and decreasing the levels of NO, MDA and oxygen free radicals.