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目的:研究肾血管性高血压(RVH)大鼠心肌肥厚及结缔组织生长因子(CTGF)的表达情况,探讨缬沙坦逆转左室重构的可能机制。方法:用两肾一夹方法构建RVH大鼠模型。以左心室重量(LVW)、LVW与体重比值(LVW/BW)作为心肌肥厚的指标,分别应用RT-PCR法和免疫组织化学染色法检测CTGF的mRNA和蛋白质的表达。结果:①RVH大鼠术后第8周出现心肌肥厚,第12周进一步加重。缬沙坦治疗后,心肌肥厚明显减轻(P<0.01)。②RVH未治疗组CTGF mRNA及蛋白表达与假手术组比较显著增加;缬沙坦治疗4或8周后,其表达较相应未治疗组显著降低(P<0.05)。结论:RVH大鼠CTGF表达增多,缬沙坦能部分抑制其过度表达。这可能是AT受体阻滞剂预防或逆转心肌肥厚重构的机制之一。
Objective: To investigate the expression of cardiac hypertrophy and connective tissue growth factor (CTGF) in renovascular hypertensive rats (RVH) and to explore the possible mechanism of valsartan in reversing left ventricular remodeling. Methods: RVH rat model was constructed by two kidneys and one clip method. Left ventricular weight (LVW) and LVW / BW (LVW / BW) were used as indexes of cardiac hypertrophy. The expressions of CTGF mRNA and protein were detected by RT-PCR and immunohistochemical staining respectively. Results: ①VHH rats developed cardiac hypertrophy in the 8th week after operation, and further increased in the 12th week. After valsartan treatment, myocardial hypertrophy was significantly reduced (P <0.01). ② The expression of CTGF mRNA and protein in RVH untreated group was significantly increased compared with that in sham operation group. After valsartan treatment for 4 or 8 weeks, the expression of CTGF mRNA and protein was significantly lower than those in untreated group (P <0.05). Conclusion: The expression of CTGF increased in RVH rats. Valsartan could partially inhibit its overexpression. This may be one of the mechanisms by which AT receptor blockers prevent or reverse myocardial hypertrophy remodeling.