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作 者:辛平[1] 魏盟[1] 黄石安[2] 李志根[2] 朱伟[1] 陈灿[2]
机构地区:[1]上海交通大学附属第六人民医院心内科,上海200233 [2]广东医学院附属医院心内科
出 处:《临床心血管病杂志》2010年第5期385-388,共4页Journal of Clinical Cardiology
摘 要: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 effects of Atorvastatin on cardiac sympathetic nerve remodeling after myocardial infarction in rats.Method:Twenty-four rats were randomly divided into three group groups: Group A(Sham group);Group B(Hyperlipemia combined with myocardial infarction group);Group C(Atorvastatin group).Hyperlipemia model was created by fat milk intragastric administration.After that,left anterior descending coronary artery was ligated to creat acute myocardial infarction.Immunohistochemical technique was used to detect the distribution and density of growth associated protein-43(GAP-43) and tyrosine hydroxylase(TH) positive staining nerve fibers at peri-infarct zone after myocardial infarction.Nerve growth factor(NGF) and interleukin-1(IL-1) protein expression was assessed by Western blotting.Indexs of oxidative stress were measure by biochemical methods.Result:Compared with A group,the densities of both GAP-43 and TH positive staining nerve fibers were significantly higher at peri-infarct zones in group B(P〈0.05 for both).In addition,group B demonstrated an upregulated NGF and IL-1 protein expression as well as an elevated level of oxidative stress(P〈0.05 for both).However,the density of both GAP-43 and TH positive staining nerve fibers were decreased at corresponding zone in group C after Atovastatin administrated for four weeks(GAP-43,4320 562;TH,3645 309,both P〈0.05).The attenuated protein express of NGF and IL-1 were detected in group C,which also demonstrated a reduction in oxidative stress(P〈0.05 for all).Conclusion:Atorvastatin could effectively improve cardiac sympathetic nerve remodeling after myocardial infarction in rats with hyperlipemia.The amelioration of oxidative stress and down-regulation of NGF protein expression exerted by atovastatin may be attributable to the improvement in cardiac sympathetic nerve remodeling.
分 类 号:R542.2[医药卫生—心血管疾病]
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