摘要
目的：观察过氧化物酶体增殖物激活受体γ（PPARγ）激动剂罗格列酮对自发性高血压大鼠（SHR）心、肾、动脉血管基质金属蛋白酶2（MMP-2）表达及活性的影响，探讨罗格列酮心血管保护作用的机制。方法：健康雄性12周龄SHR大鼠12只，体重245～255g，随机被分为2组：对照组及罗格列酮组（5mg／kg·d），每组6只。应用实时多聚酶链氏反应（PCR）、Western印迹法、明胶酶谱法（zymography）等方法对用药4周后的SHR心、肾、动脉MMP-2的表达进行测定。结果：罗格列酮治疗能使SHR心、肾MMP-2 mRNA的表达降低97．6％和58．9％（P〈0．01，P〈0．05），使胸主动脉、颈动脉MMP-2的活性降低30．7％和24．6％（P〈0．05），而蛋白表达无明显差异。结论：罗格列酮治疗逆转SHR靶器官损害的作用机制可能与降低MMP-2的作用有关。
Objective： To investigate the effect of peroxisome proliferator-activated receptor γ（PPARγ） agonist-rosiglitazone on the expression and activity of matrix metalloproteinase 2 （MMP-2） in heart, renal and artery of spontaneously hypertensive rats （SHR）. Methods： The 12 male SHR aged twelve weeks, with body weight of 245-255 g, were randomly divided into two groups： control group and rosiglitazone treated group （rosiglitazone 5 mg/kg · d, intragastric administration） （n= 6 in each group） . After four-week treatment, the expression and activity of MMP-2 in left ventricle, renal cortex, thoracic aorta and carotid artery of all the rats were determined by real time PCR, Westernblot and zymography. Results： After rosiglitazone therapy, the expression of MMP-2 mRNA in left ventricle and renal cortex decreased by 97.6% and 58.9% （P〈0.01, 〈0.05, respectively）, and the activity of MMP-2 in thoracic aorta and carotid artery decreased by 30.7% and 24.6% （P〈0.05）. Conclusion： Rosiglitazone can obviously attenuate the expression and activity of MMP-2, and may be by this way reduces remodeling in SHR.
出处
《心血管康复医学杂志》
CAS
2008年第4期338-341,344,共5页
Chinese Journal of Cardiovascular Rehabilitation Medicine
基金
上海市科委生物医药基金(No.044119657)
上海市卫生局重点专科建设项目(No.05II028)
