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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。
Objective: To investigate the effect and mechanism of Tongxinluo on endometrial lesions after vascular adventitial injury. Methods: Eighteen New Zealand white rabbits with pure hyperlipidemia were randomly divided into control group, Tongxinluo group and atorvastatin group. The rabbits were randomly divided into control group, Tongxinluo group and atorvastatin group. The control group was given saline and the other two groups were given Tongxinluo and atorvastatin for intervention, a total of 12 weeks. HE staining was used to examine the morphological changes of the adventitial lesion. The expression of α-actin, CD68 and collagen type I and III in vascular tissue was detected by immunohistochemical staining. Real-time quantitative PCR RQ-PCR) was used to detect the expression of NADPH oxidase subunit p22phox mRNA in the vascular tissue after epicardial injury. Results: Compared with the control group, Tongxinluo and atorvastatin could significantly inhibit the formation of endometrial lesions and significantly increase the expression of α-actin and collagen types Ⅰ and Ⅲ (P <0.05), and inhibit the expression of p22phox mRNA expression (P <0.05). Conclusion: Tongxinluo and atorvastatin can effectively inhibit the formation of endometrial lesions after vascular adventitia injury and increase the stability of the lesions. Antioxidant stress may be the mechanism of the two drugs.