从急性多发性脑梗死大鼠海马缺血损伤探讨毒损脑络机制

Mechanism of Toxin Damaging Brain Collaterals in Rats with Hippocampus Ischemia of Acute Multi-infarction

关键词:  急性多梗  能量代谢  自由基  毒损脑络

Key words:  acute multiple cerebral infarction model  energy metabolism  free radical  toxin damaging brain collaterals

摘要:

[目的]从能量代谢障碍、酸中毒、自由基损伤等急性脑缺血级联反应的过程及中药对其调节作用入手,探讨毒损脑络的理论观点。[方法]采用同种系微栓子体外注入法制备大鼠急性多发性脑梗死模型,缺血72h后断头取脑,常规苏木精-伊红(HE)染色光镜下观察患侧海马CA1区病理形态学改变,采用比色法测定海马组织中Na⁺-K⁺-ATP酶活性、乳酸脱氢酶(LDH)活力、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。[结果]急性多发性脑梗死大鼠模型海马CA1区出现明显缺血性形态改变,模型组海马组织中Na⁺-K⁺-ATP酶、LDH及SOD活性显著降低(P<0.01),而中药组较模型组显著升高(P<0.01);模型组海马组织中MDA含量明显增多(P<0.05),而中药组较模型组明显减少(P<0.01)。[结论]在急性脑缺血损伤过程中,能量代谢障碍、酸中毒、自由基损伤等级联反应重要环节,为毒损脑络机制提供了病生理学依据。

Abstract:

[Objective] To explore the theory of toxin damaging brain collaterals based on the cascade reaction in acute brain ischemia,including disturbance of energy metabolism,acidosis and free radical injury and the regulative effect of traditional Chinese medicine.[Methods] Acute multiple cerebral infarction was induced by injection of homologous microemboli.72 hours after ischemia the rats were killed and the brain samples with ischemia were obtained.The pathologic changes of the CA1 region of hippocampus were examined after HE staining light microscopically.The activity of Na⁺-K⁺-ATPase,lactate dehydrogenase(LDH),malondialdehyde(MDA)and superoxide dismutase(SOD)in the hippocampus tissue was measured with colorimetric determination.[Results] The morphologic changes of ischemia in CA1 region of hippocampus in rats with acute multiple infarction were obvious.The activity of the Na⁺-K⁺-ATPase,LDH and SOD of hippocampus tissue in model group was obviously decreased(P<0.01).However,in the TCM group it was obviously higher than that in model group(P<0.01).The MDA content of model group markedly increased in hippocampus tissue(P<0.05),but in the TCM group it obviously decrease when compared with model group(P<0.01).[Conclusions] In the course of acute brain ischemia injury the important cascade reaction,including disturbance of energy metabolism,acidosis and free radical injury has provided the pathologic and physiologic foundation for the mechanism study of toxin damaging brain collaterals.