论文部分内容阅读
目的观察过氧化物酶体增殖物激活受体-γ(peroxisome proliferator activated receptors-γ,PPAR-γ)在高血压血管平滑肌细胞(VSMC)表型转化中的作用。方法应用基因重组技术使PPAR-γ过表达和表达抑制,Western blot方法检测分化型VSMC标志物α-SMA和未分化型VSMC标志物OPN的蛋白表达,应用DNA合成率检测和细胞计数的方法测定细胞增殖率,常规病理切片和HE染色观察血管形态学改变。结果PPAR-γ激动剂罗格列酮可降低SHR大鼠血压,并改善主动脉血管重构。②SHR大鼠主动脉中OPN表达增多而α-SMA表达减少,应用罗格列酮可抑制上述改变。③SHR大鼠来源的VSMC中OPN表达增多而α-SMA表达减少,细胞增殖率升高,PPAR-γ过表达使细胞增殖率降低,并抑制OPN和α-SMA的表达改变。结论PPAR-γ可抑制高血压VSMC向未分化表型的转化,可能是其改善高血压血管重构的重要机制。
Objective To investigate the role of peroxisome proliferator activated receptors-γ (PPAR-γ) in the phenotypic transformation of vascular smooth muscle cells (VSMCs) in hypertensive rats. Methods The overexpression and expression of PPAR-γ were inhibited by gene recombination technique. Western blot was used to detect the protein expression of α-SMA, a differentiated VSMC marker, and OPN, an undifferentiated VSMC marker. The rate of DNA synthesis and cell counting were determined Cell proliferation rate, routine pathological sections and HE staining were observed vascular morphological changes. Results Rosiglitazone, a PPAR-γ agonist, reduced blood pressure and ameliorated aortic remodeling in SHR rats. ② In the aorta of SHR rats, the expression of OPN increased while the expression of α-SMA decreased. Rosiglitazone could inhibit the above changes. ③ The expression of OPN and α-SMA in VSMC derived from SHR rats increased but the proliferation rate of cells increased. PPAR-γ overexpression decreased the proliferation rate and inhibited the expression of OPN and α-SMA. Conclusion PPAR-γ can inhibit the conversion of hypertensive VSMC to undifferentiated phenotype, which may be an important mechanism of improving vascular remodeling of hypertension.