论文部分内容阅读
目的:探讨普萘洛尔对肾上腺素促大鼠动脉粥样硬化斑块进展的预防作用及其机制。方法:50只Wistar雄性大鼠经高脂喂养17周,制成动脉粥样硬化模型。随机分为对照组、肾上腺素组、普萘洛尔小剂量组、普萘洛尔中剂量组、普萘洛尔大剂量组,每组10只。所有大鼠在继续高脂喂养基础上,对照组皮下注射生理盐水0.5ml/d;肾上腺素组予肾上腺素0.5mg.kg-1.d-1皮下注射;普萘洛尔小、中、大剂量组分别予普萘洛尔2.5mg.kg-1.d-1、5mg.kg-1.d-1、7.5mg.kg-1.d-1灌胃,0.5h后皮下注射肾上腺素0.5mg.kg-1.d-1。分组处理1周,处死全部大鼠,取主动脉粥样斑块用免疫组织化学方法检测巨噬细胞(CD68)浸润及MMP-9表达。结果:肾上腺素组,CD68阳性细胞浸润及MMP-9的表达显著高于对照组;普萘洛尔小、中、大剂量组,CD68阳性细胞浸润程度及MMP-9的表达较肾上腺素组显著减少,且减少程度与普萘洛尔剂量呈正相关。结论:普萘洛尔可以减轻肾上腺素刺激后大鼠动脉粥样硬化斑块内巨噬细胞的浸润及其MMP-9表达,有延缓肾上腺素促大鼠动脉粥样硬化斑块进展的作用。
Objective: To investigate the prophylactic effect of propranolol on the progression of atherosclerotic plaque in rats and its mechanism. Methods: Fifty male Wistar rats were fed with high fat diet for 17 weeks to make the model of atherosclerosis. Randomly divided into control group, epinephrine group, propranolol small dose group, propranolol middle dose group, propranolol high dose group, 10 rats in each group. On the basis of continuing high-fat feeding, the control group was subcutaneously injected with normal saline (0.5ml / d); epinephrine (0.5mg.kg-1.d-1) was given subcutaneously; propranolol was small, medium and large Dose group were given propranolol 2.5mg.kg-1.d-1, 5mg.kg-1.d-1, 7.5mg.kg-1.d-1 gavage 0.5h subcutaneous injection of epinephrine 0.5 mg.kg-1.d-1. One week after the treatment, all the rats were sacrificed, and the aortic plaque was used to detect the infiltration of macrophages (CD68) and the expression of MMP-9 by immunohistochemistry. Results: The infiltration of adrenaline group and CD68 positive cells and the expression of MMP-9 were significantly higher than those of the control group. The infiltration of CD68 positive cells and the expression of MMP-9 in small, medium and large doses of propranolol group were significantly higher than those in the adrenaline group Reduce, and reduce the degree of propranolol dose was positively correlated. CONCLUSIONS: Propranolol can reduce the infiltration of macrophages and the expression of MMP-9 in atherosclerotic plaques of rats after epinephrine stimulation and delay the progression of atherosclerotic plaques induced by adrenaline in rats.