摘要
本实验给大鼠腹腔注射生脉散注射液(0.25ml/100g),观察脑缺血60min后再灌流60min脑电图、脑含水量和脑组织丙二醛含量的变化.结果为;脑缺血30min起,脑电图开始有恢复,至再灌60min恢复到对照的1/4;脑含水量生脉散组明显低于再灌组(P<0.05);脑组织丙二醛含量生脉散组明显低于再灌组(p<0.01).结果表明生脉散注射液对大鼠全脑缺血再灌流损伤有保护作用,其机理与抑制脂质过氧化有关.
Shengmai San is a Chinese traditional medical prescription. In this study,we observed the influence of Shengmai San injection on electroencephalography,cerebral water content and malondialdehyde (MDA ) content of cerebral ischemia-reperfusion in rats and explored its mechanisms. Wister rats were used in this study. The cerebral ischemia-reperfusion model was produced by clipping basilar artery and bilateral common carotid arteries for 60 minutes and then reopenning three vessels with 60 minutes reperfusion. Shengmai San was Injected intraperitoneally in 0. 25ml/100g body weight in 30 minutes before clipping three vessels. Electroencephalography, cerebral water content and malondialdehyde content were determined. The result showed: In 30 minutes after clipping three vessels. electroencephalography recovered mildly. Its amplitude was one fourth of control in 60 minutes after reperfusion. Cerebral water contents in control,cerebral ischemia-reperfusion and Shengmai San groups were 78. 32±0. 06,80. 52±0.05 and 78. 86±0. 01 (%) respectively.Compared with ischemia-reperfusion group,cerebral water content in Shengmai San group was significantly lowered ( P <0. 05). Malondialdenhyde (MDA) contents in rat brain in control ,cerebral ischemia-reperfusion and Shengmai San groups were 5. 19±0. 51,6. 34±0. 62 and 4. 84±0. 93(nmol/mg wet weight) respectively. Compared with ischemia-reperfusion group, malondialdehyde (MDA) content was significantly lowered ( P <0. 01). These results demonstrated that Shengmai San injection can protect signficantly against reperfusion damage following cerebral ischemia in rats,and that its mechanisms are correlated with depression of lipid peroxida-tion.
出处
《蚌埠医学院学报》
CAS
1993年第2期120-123,共4页
Journal of Bengbu Medical College
基金
安徽省教育委员会资助
关键词
生脉散
脑缺血
再灌注损伤
针剂
Shengmai San
cerebral ischemia-reperfusion damage
lipid peroxidation
oxygen free radical
rat
