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目的:研究新型ATP敏感性钾通道开放剂埃他卡林(IPT)对低氧性肺动脉高压(HPH)大鼠肺动脉血管内皮生长因子(VEGF)表达的影响。方法:雄性SD大鼠36只随机分成对照组、HPH模型组、IPT干预组,每组12只。IPT干预组给予IPT1.5mg/(kg.d)灌胃,对照组及HPH模型组给予0.9%NaCl5ml/(kg.d)灌胃。HPH组及IPT干预组在(10.0±0.5)%氧浓度下饲养,每天8h,每周6天,4周时测定平均肺动脉压(mPAP)、RV/(LV+S),逆转录聚合酶链式反应(RT-PCR)和Western-blot技术检测各组肺动脉主干VEGF mRNA和蛋白的表达。结果:①HPH模型组大鼠mPAP和RV/(LV+S)显著高于对照组(P<0.01),IPT干预组mPAP和RV/(LV+S)较HPH模型组显著下降(P<0.01)。②HPH模型组大鼠肺动脉VEGF mRNA及蛋白表达高于对照组,两者具有显著统计学意义(P<0.01),IPT干预组与HPH模型组比较,VEGF mRNA及蛋白表达均下降(P<0.01);IPT干预组与对照组比较,VEGF mRNA及蛋白表达差异无显著性(P>0.05)。结论:HPH模型大鼠肺动脉VEG FmRNA及蛋白表达增加,IPT可明显抑制慢性低氧大鼠肺动脉VEGFmRNA和蛋白的表达。
AIM: To investigate the effect of IPT, a novel ATP-sensitive potassium channel opener, on the expression of vascular endothelial growth factor (VEGF) in rats with hypoxic pulmonary hypertension (HPH). Methods: Thirty-six male SD rats were randomly divided into control group, HPH model group and IPT intervention group, with 12 rats in each group. IPT intervention group given IPT1.5mg / (kg.d) intragastric administration, control group and HPH model group given 0.9% NaCl5ml / (kg.d) gavage. HPH group and IPT intervention group were fed at the oxygen concentration of (10.0 ± 0.5)%, and the mean pulmonary arterial pressure (mPAP), RV / (LV + S), and reverse transcription polymerase chain The expressions of VEGF mRNA and protein in the main pulmonary arteries were detected by RT-PCR and Western-blot respectively. Results: ① The levels of mPAP and RV / (LV + S) in PHA group were significantly higher than those in HPH group (P <0.01) . (2) Compared with HPH model group, the expression of VEGF mRNA and protein in pulmonary arteries of HPH model group was significantly higher than that of control group (P <0.01) There was no significant difference in the expression of VEGF mRNA and protein between the IPT intervention group and the control group (P> 0.05). CONCLUSION: The expression of VEGF mRNA and protein in pulmonary arteries of HPH model rats is increased. IPT can significantly inhibit the expression of VEGF mRNA and protein in pulmonary arteries of rats with chronic hypoxia.