灯盏生脉胶囊对大鼠脑缺血及再灌注损伤的影响

Study in effects of Dengzhanshengmai capsules on cerebral ischemia and reperfusion injury in rats

目的:观察灯盏生脉胶囊对大鼠脑缺血及再灌注损伤的作用并探讨其作用机制。方法:将80只大鼠随机分为假手术1组、假手术2组、生理盐水对照组、灯盏生脉胶囊低剂量组、灯盏生脉胶囊高剂量组,每组16只。采用改良的ZeaLonga线栓法制作大鼠大脑中动脉阻塞模型,缺血前后口服灯盏生脉胶囊,进行神经病学评分,检测凝血酶原时间(PT)、纤维蛋白原(Fg)、血小板最大聚集率等血液学指标以及血浆内皮素(ET)、血清一氧化氮(NO)水平,并测量脑梗死体积、脑水肿体积、脑组织中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。结果:灯盏生脉胶囊低剂量组和高剂量组大鼠脑缺血再灌注2h及24h,神经病学评分均低于生理盐水对照组(1.75±0.68、1.71±0.77对2.35±0.86;1.88±0.81、1.71±0.69对2.65±1.17,P<0.05);灯盏生脉胶囊高剂量组大鼠PT较生理盐水对照组延长(18.0±0.8s对17.0±0.6s,P<0.05),ET含量则低于生理盐水对照组(13.9±4.9pg/ml对26.3±13.2pg/ml,P<0.05);灯盏生脉胶囊低剂量组和高剂量组大鼠脑梗死体积比及脑水肿体积比均低于生理盐水对照组(10.3±3.8%、9.7±5.7%对11.9±3.0%,7.7±3.0%、6.9±3.9%对18.3±7.0%,P<0.05);灯盏生脉胶囊低剂量组和高剂量组大鼠脑组织SOD活性均高于生理盐水对照组(291±78U/mg、301±92U/mg对213±40U/mg,P<0.05),MDA含量则明显低于生理盐水对照组(1.41±0.47nmol/mg、1.36±0.61nmol/mg对2.09±0.32nmol/mg,P<0.05,P<0.01);其余指标的差异无统计学意义(P>0.05)。结论:灯盏生脉胶囊具有防治大鼠脑缺血及缺血再灌注损伤的作用,其作用机制可能为提高抗氧化酶活性,抑制脂质过氧化反应、减少自由基对脑组织的损害,以及抑制凝血、降低血管阻力等。

Objective. To observe the effect of Dengzhanshengmai capsules on cerebral ischemia and reperfusion injury in rats, and discuss its mechanism. Methods： Eighty rats were divided into 5 groups： sham-operated group 1, sham-operated group 2, saline control group, low-dose Denszhanshengmai group, and high-dose Denszhanshengmai group. Each group had 16 rats. The middle cerebral artery occlusion model in rats were made by the modified suture-occluded method of Zea longa. The rats were administrastion with Dengzhanshengmai capsules orally before and after cerebral ischemia. Neurological score was carried out. Some haematological indexes （such as prothrombin time, fibrin content, and maximum agglutination rate of platelets）, plasma endothelin level, and serum nitrogen oxide level were measured. The size of crebral infarct and edema, the activity of SOD, and the content of MDA were measured as well. Results： The neurological score in the low-dose and high-dose Denszhanshengmai groups after 2 and 24 hours reperfusion was lower than those of the control group （1.75±0.68, 1.71±0.77 vs2.35±0.86, 1.88±0.81, 1.71±0.69 vs2.65±1.17, P〈0.05）. The PT in the high-dose Denszhanshengmai group was longer than that of the saline control group （18.0±0.8s vs17.0±0.6s, P〈0.05） while the level of ET was lower （13.9±4.9 pg/ml vs 26.3±13.2, P〈0.05）. The infarct size and edema size in the Denszhanshengmai group were smaller than those of the saline control group （10.3±3.8%. 9.7±5.7% vs11.9±3.0%, 7.7±3.0%, 6.9±3.9% vs 18.3±7.0%, P〈0.05）, The activity of SOD in the Denszhanshengmai group was higher than that of the saline control group （291±78 U/mg, 301±92U/mg vs213±40 U/mg, P〈 0.05） while the content of MDA was much lower （1.4±0.47nmol/mg. 1.36±0.61nmol/mg vs 2.09±0.32 nmol/mg, P〈0.05, P〈0.01）. But no significant differences were found in the levels of Fg, maximum aggregation of platelets, and nitrogen oxide. Conclusion： Dengzhanshengmai capsules is effective for preventing and treating cerebral ischemia and reperfusion injury. The mechanisms of its effect may be associated with improving the activities of antioxidases, suppressing lipid peroxidation, alleviating the injuries induced by free radicals, suppressing blood agglomeration,and reducing blood vessel resistance.