内毒素对大鼠动脉粥样硬化病灶的影响及TLR4的作用

目的探讨慢性炎症过程对大鼠动脉粥样硬化形成的影响。方法本实验通过定期腹腔注射小剂量细菌内毒素的方法在高脂饲养的大鼠体内引起一个持续性的低水平的全身炎症反应,以促进了大鼠冠状动脉及主动脉的血管病变,根据处理因素的不同把动物分为正常组(A组)、单独内毒素注射组(B组)、单独高脂饲养组(C组)和内毒素注射 高脂饲养组(D组),分别在2、4、8、12周时杀死动物采血并留取组标本。HE染色观察主动脉内膜变化情况,免疫组织化学检测观察主动脉内皮TLR4的表达情况。结果①D组大鼠主动脉动脉内皮下泡沫细胞的出现较其他组提前,主动脉及冠状动脉的变化以平滑肌细胞增生、动脉管腔狭窄为主,部分符合动脉粥样硬化的病理变化,且动脉形态学变化较其他组更显著。②A组大鼠主动脉内皮细胞无TLR4表达,B组、C组和D组大鼠主动脉内皮细胞有TLR4表达,且D组升高的程度明显高于内毒素组和高脂饲养组。结论慢性炎症过程对大鼠动脉粥样硬化的形成具有显著促进作用,此过程可能是由TLR4受体介导的。

Effects of LPS on development of atherosclerosis and role of TLR4

Objective To investigate the effects of chronic inflammation, induced by LPS on the development of rat aorta atherosclerosis. Methods Eighty healthy male Wistar rats were divided into 4 groups, normal control, the endotoxin group, homofat-breeded group and endotoxin-homofat-breeded group. HE staining was used to detect the change of rat aorta endomembrane and immunohistochemistry was used to detect the change of expression of TLR4 in rat aorta endothelial cell. Results The AS animal model was constructed successfully and the expression of TLR4 was at a higher level in endotoxin-homofat-breeded group than that in other groups. Conclusion Chronic inflammation has an actively effect during the development of rat aorta atherosclerosis.