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机构地区:[1]济南军区青岛第一疗养院疗养科,山东青岛266071 [2]第二军医大学长征医院心血管内科,上海200003
出 处:《心脏杂志》2012年第5期573-577,共5页Chinese Heart Journal
摘 要:目的:探讨通心络对血管外膜损伤后内膜病变的作用及机制。方法:纯种高血脂新西兰大白兔18只,采用胶原酶消化+钝性机械分离的方法建立兔颈动脉外膜损伤模型后,随机分为对照组、通心络组和阿托伐他汀组,对照组给予盐水灌胃,另两组分别给予通心络和阿托伐他汀进行干预,共12周。采用HE染色法检查外膜损伤血管的形态变化,用免疫组化染色法测定血管组织中α-actin、CD68及Ⅰ、Ⅲ型胶原蛋白的表达;用实时荧光定量PCR(real-time quantitative PCR,RQ-PCR)技术检测外膜损伤后血管组织中NADPH氧化酶亚单位p22phox mRNA的表达。结果:与对照组比较,通心络和阿托伐他汀均可显著抑制内膜病变的形成,并明显增加病变中α-actin及Ⅰ、Ⅲ型胶原蛋白的表达(P<0.05),抑制p22phox mRNA的表达(P<0.05)。结论:通心络及阿托伐他汀均可有效地抑制血管外膜损伤后内膜病变的形成,并增加病变的稳定性,抗氧化应激可能是两种药物作用的机制。AIM: To investigate the effects of tongxinluo (TXL) on intimal hyperplasia lesions induced by adventitial injury and the possible mechanism. METHODS: Models of vascular adventitial injury were established by combining collagenase digestion and mechanical dissection after a 2-week high-cho- lesterol diet. TXL group and atorvastatin group received the respective drugs for 12 weeks. HE staining was used to examine morphological changes in vessels after adventitial injury and immunohistochemical staining was used to detect the expressions of α-actin, CD68, collagen I and collagen III. RQ-PCR was used to measure expressions of mRNA of p22phox, a subunit of NADPH oxidase. RESULTS : Both TXL and atorvastatin inhibited intimal lesions significantly. Compared with those in the control group, expressions of ct-actin, collagen I and collagen III increased in both TXL group and atorvastatin group, but expression of mRNA of p22phox was reduced significantly. CONCLUSION : Tongxinluo reduces and stabilizes intimal hyperplasia lesions induced by adventitial injury, possibly through inhibiting oxidative stress.
关 键 词:血管外膜 内膜病变 NADPH 氧化酶 动脉粥样硬化 通心络
分 类 号:R543.5[医药卫生—心血管疾病]
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