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目的对比罗格列酮或氯沙坦及二者合用对大鼠胸主动脉损伤后再狭窄的影响,并探讨其分子生物学机制。方法以球囊损伤方法建立大鼠胸主动脉损伤模型。雄性SD大鼠随机分成(1)假手术组,(2)罗格列酮组,(3)氯沙坦组,(4)罗格列酮+氯沙坦组,(5)损伤组。7d后光镜和HE染色观察血管管腔面积和内膜面积变化,以原位杂交方法检测基质金属蛋白酶9(MMP9)mRNA的表达,以免疫组化方法检测MMP9及磷酸化细胞外信号调节激酶1/2(pERK1/2)蛋白表达;术后4h,1d和7d,以放射免疫法检测血浆中肿瘤坏死因子α(TNFα)变化。结果罗格列酮+氯沙坦组明显抑制动脉再狭窄,抑制MMP9mRNA及蛋白表达以及pERK1/2蛋白表达,降低血浆中TNFα浓度。而罗格列酮组和氯沙坦组不能抑制动脉狭窄及MMP9和pERK1/2表达。结论罗格列酮与氯沙坦二者合用可以显著抑制大鼠主动脉损伤后再狭窄,降低MMP9及pERK1/2表达,使血浆中炎症因子减少。
Objective To compare the effects of rosiglitazone or losartan and their combination on restenosis after thoracic aorta injury in rats and to explore its molecular biological mechanism. Methods A rat model of thoracic aorta injury was established by balloon injury. Male Sprague-Dawley rats were randomly divided into sham operation group, rosiglitazone group, losartan group, rosiglitazone + losartan group and injury group. The expression of MMP9 mRNA was detected by light microscopy and HE staining 7 days later. The expressions of MMP9 and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1 / 2) protein expression was detected by radioimmunoassay at 4h, 1d and 7d after operation. The plasma levels of TNFα were detected by radioimmunoassay. Results Rosiglitazone plus losartan significantly inhibited arterial restenosis, inhibited MMP9 mRNA and protein expression and pERK1 / 2 protein expression, and decreased plasma concentrations of TNFα. The rosiglitazone group and losartan group can not inhibit arterial stenosis and MMP9 and pERK1 / 2 expression. Conclusion Rosiglitazone combined with losartan can significantly inhibit the restenosis of rat aorta after injury, reduce the expression of MMP9 and pERK1 / 2, and decrease the plasma inflammatory cytokines.