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目的:探讨阿托伐他汀对急性心肌梗死(AMI)大鼠交感神经重构的影响。方法:24只SD大鼠随机分为3组:A组(假手术组);B组(AMI合并血脂异常组);C组(阿托伐他汀干预组)。采用结扎冠状动脉前降支,结合喂饲高脂饮食制作AMI合并血脂异常模型,免疫组化法检测各组大鼠梗死周边区生长相关蛋白-43(GAP-43)和酪氨酸羟化酶(TH)阳性神经纤维分布和密度,Western blot方法检测神经生长因子(NGF)和白细胞介素-1β(IL-1β)蛋白表达。生化法检测氧化应激相关指标。结果:与A组比较,B组梗死周边区域GAP-43和TH阳性神经纤维密度明显增加(均P<0.05),NGF和IL-1β蛋白表达增加(均P<0.05),伴随氧化应激水平增高(P<0.05)。C组GAP-43和TH阳性神经纤维密度较B组显著减少(均P<0.05),伴随NGF、IL-1β蛋白表达降低(均P<0.05)及氧化应激状态的改善。结论:阿托伐他汀可有效的改善AMI合并血脂异常大鼠交感神经重构,其机制与氧化应激状态改善和NGF表达下调有关。
Objective: To investigate the effect of atorvastatin on sympathetic remodeling in rats with acute myocardial infarction (AMI). Methods: Twenty-four SD rats were randomly divided into three groups: group A (sham operation group), group B (AMI combined with dyslipidemia group) and group C (atorvastatin intervention group). The model of AMI with dyslipidemia was established by ligating the anterior descending coronary artery and feeding high-fat diet. The expression of growth-associated protein-43 (GAP-43) and tyrosine hydroxylase (TH) positive nerve fiber distribution and density, Western blot was used to detect the expression of nerve growth factor (NGF) and interleukin-1β (IL-1β). Biochemical detection of oxidative stress related indicators. Results: Compared with group A, the density of GAP-43 and TH-positive nerve fibers in peripheral area of group B increased significantly (all P <0.05) and the expression of NGF and IL-1β increased Increased (P <0.05). The density of GAP-43 and TH-positive nerve fibers in group C was significantly lower than that in group B (all P <0.05), accompanied with the decrease of NGF and IL-1β protein (P <0.05) and the improvement of oxidative stress. Conclusions Atorvastatin can effectively improve the sympathetic nerve remodeling in AMI rats with dyslipidemia. The mechanism is attributed to the improvement of oxidative stress and the down-regulation of NGF expression.