高脂高糖家兔脑梗死模型基底膜损伤机制的探讨

Mechanism of basement membrane injury in cerebral infarction model in rabbit with hyperglycemia and hyperlipidemia

目的探讨脑缺血后微血管内皮细胞基底膜的损伤机制。方法24只新西兰家兔采用随机数字表法分为非高脂高糖脑梗死模型对照组（简称空白对照组），高脂高糖脑梗死模型对照组（简称模型对照组），每组12只。空白对照组给予普通饲料，模型对照组给予高脂高糖饲料，均制作成脑梗死模型。监测造模前后血浆中层粘连蛋白（LN）的表达，并观察脑组织中LN表达情况。结果模型对照组高脂高糖模型制作后，家兔血脂血糖增高，与造模前比较差异有统计学意义（P〈0．05）。脑梗死模型制作后两组血浆中LN表达减少，与造模前比较差异有统计学意义（P〈0．05）。病理观察结果显示LN主要表达在微血管基质，阳性反应为黄色到棕褐色。结论兔脑梗死模型中早期即有微血管内皮细胞基底膜的损伤，表现在细胞外基质中LN的降低。在脑缺血早期积极干预患者血糖血脂水平及联合运用脑保护剂、MMPs抑制剂将有效改善梗死程度。

Objective To discuss the mechanism of microvascular endothelial basement membrane injury following cerebral ischemia. Methods Twenty-four New Zealand rabbits were randomly divided into two groups （n=12）： normal control group and model group. The latter were fed high-fat, high-sucrose diet, but the former was fed with normal diet. They all were made into the models of cerebral infarction. The change of Laminin （LN） in blood and the expression of LN in brain tissue were observed simultaneously. All groups received pathological examination. Results The levels of blood lipids and blood glucose of rabbit and the content of LN were significantly increased after fed with high fat and high sucrose about 1-2 times in 10 d. The plasma concentration of LN was decreased significantly after the operation of cerebral infarction （P〈0.05）. Pathological observation revealed that LN was mainly located in cytoplasm of microvascular matrix, and its positive reaction was yellow to brown. Conclusions Injury of the microvascular endothelial basement membrane exists in the early phase of rabbit cerebral ischernia, leading to decrease of LN in extracellular matrix. The early intervention of blood lipids and blood glucose, accompanied by the brain protection with agents and the application of inhibitors of MMPs, will be able to effectively improve the cerebral infarction.