基质金属蛋白酶-9在高血压大鼠血管重塑中表达及替米沙坦的干预作用

目的 探讨基质金属蛋白酶-9（MMP-9）在双肾一夹型高血压大鼠血管重塑中的表达及其可能的凋节机制.方法 将雄性wistar大鼠随机分成三组,假手术对照组（n=10）,双肾一夹型模型组（n=10）,替米沙坦（telmisartan）组,即治疗组（n=7）,治疗组给予每天灌胃,三组均在术后每周监测血压,8周后处死大鼠取胸主动脉与颈总动脉作形态学观察,免疫组化法检测颈总动脉与胸主动脉MMP-9的蛋白表达.结果 与对照组相比,模型组血压明显升高（P＜0.05）,颈总动脉与胸主动脉模型组管壁增厚,MMP-9表达显著增加.治疗8周后,治疗组血压明显降低,管壁变薄,MMP-9表达减少.结论 MMP-9可能与高血压血管重塑有关,替米沙坦通过降低血压抑制血管中MMP-9的表达,并改善血管重塑.

Expression of MMP-9 and the intervention effect of telmisartan on vascular remodeling of 2K1C Hypertension Rats

Objective To explore the expression and mechanisms of MMP-9 in vascular remodeling of two-kidney and one-cliped hypertension rats. Methods Male Wistar rats were randomly divided into sham operation group( n = 10), two-kidney and one-clip model (2KIC) group ( n = 10) and telmisartan group ( n = 7 ). Telmisartan group were injected with telmisartan every day. The blood pressure was determined every week. The morphologic change of carotid artery and thoracic aorta was observed with HE stainning 8 weeks after treatment with telmisartan.Arteries was performed to evaluate the expression of MMP-9 with immunohistochemisty. Results The blood pressure,vessel wall,and the expression of MMP-9 in model group were significantly higher than that of control group.Telmisartan nearly normalized arterial pressure and suppressed all these changes. Conclusion MMP-9 was related to vascular remodeling and Telmisartan could regulate vascular remodeling in 2-kidney and 1-cliped hypertension rats by inhibiting the pathway of MMP-9.