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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 Dengzhan Shengmai Capsule on cerebral ischemia and reperfusion injury in rats and to explore its mechanism. METHODS: Eighty rats were randomly divided into sham operation group 1, sham operation group 2, normal saline control group, Dengzhan Shengmai capsule low-dose group and Dengzhanshengmai capsule high-dose group, with 16 rats in each group. A rat model of middle cerebral artery occlusion was made using a modified Zea Longa line plug method. Dengzhan Shengmai capsules were taken orally before and after ischemia for neurological scores. Prothrombin time (PT), fibrinogen (Fg), and platelet maximum aggregation rate were measured. Hematological parameters, plasma endothelin (ET), serum nitric oxide (NO) levels, and cerebral infarction volume, brain edema volume, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in brain tissue were measured. . RESULTS: After 2 and 24 hours of cerebral ischemic reperfusion in rats in the low-dose and high-dose Dengzhan Shengmai capsules, the neurological scores were lower than those in the saline control group (1.75±0.68, 1.71±0.77 vs. 2.35±0.86; 1.88±0.81; 1.71±0.69 vs 2.65±1.17, P<0.05); PT in the high-dose group of Dengzhan Shengmai Capsule was prolonged compared with the saline control group (18.0±0.8s versus 17.0±0.6s, P<0.05), and the ET content was low. In the saline control group (13.9±4.9 pg/ml versus 26.3±13.2 pg/ml, P<0.05), the ratio of brain infarct volume and volume ratio of cerebral edema was lower in the rats of the low-dose group and the high-dose group of Dengzhanshengmai Capsule. Normal saline control group (10.3±3.8%, 9.7±5.7% vs 11.9±3.0%, 7.7±3.0%, 6.9±3.9% vs 18.3±7.0%, P<0.05); Dengzhan Shengmai Capsule low-dose group and high dose The activity of SOD in the rat brain was higher than that in the saline control group (291±78 U/mg, 301±92 U/mg vs 213±40 U/mg, P<0.05), and the MDA content was significantly lower than that in the saline control group (1.41). ±0.47nmol/mg, 1.36±0.61nmol/mg vs 2.09±0.32nmol/mg, P<0.05, P<0.01); the other indicators had no significant difference (P>0.05). Conclusion: Dengzhanshengmai capsule can prevent and treat cerebral ischemia and ischemia-reperfusion injury in rats. Its mechanism may be to increase antioxidative enzyme activity, inhibit lipid peroxidation, reduce free radical damage to brain tissue, and Inhibits coagulation, reduces vascular resistance, etc.