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目的通过全反式维甲酸(ATRA)在肺动脉高压大鼠中对α-平滑肌肌动蛋白(α-SMA)表达的影响,探讨ATRA治疗肺动脉高压可能机制。方法将30只雄性SD大鼠,随机分为对照组、模型组、干预组,每组10只。模型组和干预组大鼠腹腔一次性注射野百合碱,60mg/kg,制作肺动脉高压模型;干预组于制模当天起,每天一次给予ATRA灌胃,30mg/(kg·d),连续28d。第28天检测各组大鼠肺动脉平均压、右心室肥厚指数(RVHI),测定肺小动脉管壁厚度占动脉外径的百分比(WT%)及管壁面积占血管总面积的百分比(WA%)。实时荧光定量PCR和Western blot检测α-SMA mRNA及蛋白在肺组织中的表达。结果模型组大鼠的肺动脉平均压、RVHI和WT%、WA%均显著高于干预组和对照组,干预组亦均高于对照组,差异有统计学意义(P均<0.01)。模型组大鼠肺组织中α-SMA mRNA和蛋白表达水平显著高于对照组和干预组,差异有统计学意义(P<0.01),而干预组与对照组的差异无统计学意义(P>0.05)。结论 ATRA可抑制野百合碱诱导的大鼠肺动脉高压模型中肺组织α-SMA mRNA和蛋白的表达,对肺动脉高压可能有治疗作用。
OBJECTIVE: To investigate the effect of ATRA on the expression of α-smooth muscle actin (α-SMA) in pulmonary hypertensive rats and to explore the possible mechanism of ATRA for pulmonary hypertension. Methods Thirty male SD rats were randomly divided into control group, model group and intervention group, with 10 rats in each group. Rats in the model group and the intervention group were injected intraperitoneally with monocrotaline (60mg / kg) intraperitoneally to establish the pulmonary hypertension model. The intervention group was given intragastric administration of ATRA once daily for 30 days for 28 days. The mean pulmonary artery pressure and right ventricular hypertrophy index (RVHI) of the rats in each group were measured on the 28th day. The percentage of pulmonary artery wall thickness to the outside diameter of arterial artery (WT%) and the percentage of wall area to total vessel area (WA% ). Real-time fluorescence quantitative PCR and Western blot were used to detect the expression of α-SMA mRNA and protein in lung tissue. Results The pulmonary artery mean pressure, RVHI, WT% and WA% of the model group were significantly higher than those of the intervention group and the control group, and the intervention group were also higher than the control group, the difference was statistically significant (P all <0.01). The expression of α-SMA mRNA and protein in the lung tissue of the model group was significantly higher than that of the control group and the intervention group (P <0.01), but there was no significant difference between the intervention group and the control group (P> 0.05). Conclusion ATRA can inhibit α-SMA mRNA and protein expression in lung tissue induced by monocrotaline-induced pulmonary hypertension in rats and may have a therapeutic effect on pulmonary hypertension.