论文部分内容阅读
目的:观察2型糖尿病大鼠颈动脉球囊导管损伤后血管内膜血管紧张素转化酶2(ACE2)的表达,初步探讨替米沙坦对球囊导管损伤后动脉内膜增生的作用及机制,血管ACE2表达的调节作用及对其的影响。方法:30只7周龄雄性SD大鼠高糖高脂饮食4周后腹腔注射链尿佐菌素(STZ,35mg·kg-1)建成2型糖尿病大鼠模型,将建成的模型经颈外动脉行球囊损伤成功后将大鼠分成4组,每组8只:正常对照组(NC)、2型糖尿病组、单纯球囊损伤组、替米沙坦组(0.8mg·kg-1.d-1)。药物治疗2周后,用RT-PCR法测定颈动脉中ACE2mRNA的表达水平,免疫组化法比较ACE2蛋白的表达。结果:与正常SD大鼠相比,2型糖尿病大鼠颈动脉内膜ACE2mRNA及其蛋白的表达均明显降低,分别降低30.1%,57.1%(P<0.05).与糖尿病模型组比较,替米沙坦组ACE2mRNA及蛋白水平增加(P<0.01),与单纯损伤组比较ACE2mRNA和蛋白的表达亦明显增加,分别增加44.0%和63.6%(P<0.01)。结论:(1)动脉内膜ACE2表达水平的降低可能是糖尿病大鼠动脉病变的发病机制之一;(2)ARB可能是通过增加动脉内膜局部ACE2的表达而发挥血管保护作用。
OBJECTIVE: To investigate the expression of angiotensin-converting enzyme 2 (ACE2) after balloon catheter injury of carotid artery in type 2 diabetic rats and to explore the mechanism and mechanism of telmisartan on intimal hyperplasia after balloon catheter injury , Regulation of vascular ACE2 expression and its impact. Methods: Thirty male Sprague-Dawley rats, aged 7 weeks, were injected into streptozotocin (STZ, 35 mg · kg-1) intraperitoneally to establish a rat model of type 2 diabetes 4 weeks later. The rats were divided into 4 groups (n = 8): normal control group (NC), type 2 diabetes mellitus group, simple balloon injury group and telmisartan group (0.8 mg · kg -1) after balloon injury. d-1). Two weeks after the drug treatment, the expression of ACE2 mRNA in carotid artery was detected by RT-PCR and the expression of ACE2 protein by immunohistochemistry. Results: Compared with normal SD rats, the expression of ACE2mRNA and its protein in carotid intima decreased significantly in type 2 diabetic rats, which decreased by 30.1% and 57.1% respectively (P <0.05) .Compared with diabetic model group, ACE2 mRNA and protein levels were increased in the sham group (P <0.01). Compared with the simple injury group, the expression of ACE2 mRNA and protein was also increased by 44.0% and 63.6%, respectively (P <0.01). CONCLUSION: (1) The decrease of ACE2 in arterial intima may be one of the pathogenesis of arterial lesions in diabetic rats. (2) ARB may exert its vascular protective effect by increasing the expression of ACE2 in the intima of artery.