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目的探讨腺病毒介导野生型p53基因转染对高肺血流肺动脉高压大鼠肺动脉压力及平滑肌细胞的影响。方法 60只大鼠随机分为空白对照组、模型对照组、实验组和实验对照组,每组15只。模型对照组、实验组和实验对照组采用套管法连接右侧颈总动脉和颈外静脉建立高肺血流肺动脉高压大鼠模型。空白对照组仅做假手术暴露颈总动脉处理。采用气管吸入法转染携带野生型p53基因的腺病毒(Adeno-p53)至实验组,同法转染重组腺病毒载体(Adeno-lacZ)至实验对照组,病毒保存液转染至空白对照组和模型对照组。采用Western blot法分析p53基因的表达;采用右心导管测压法测定各组大鼠右室平均压(mRVP)、肺动脉平均压(mPAP);肺组织HE染色观察肺小动脉形态学改变,计算管壁厚度与血管外径比值(WT%)、凋亡指数(AI)等,评价野生型p53基因转染对大鼠肺动脉压力及平滑肌细胞凋亡的影响。结果实验组大鼠成功转染Adeno-p53后,大鼠mRVP、mPAP、RVHI、WT%低于其他三组(P<0.05),肺动脉平滑肌细胞AI高于其他三组(P<0.05)。结论 Adeno-p53基因转染能在一定程度上缓解高肺血流型大鼠肺动脉高压的发展,其机制可能与野生型p53基因可以诱导肺动脉平滑肌细胞凋亡的增加有关。
Objective To investigate the effect of adenovirus-mediated wild-type p53 gene transfection on pulmonary artery pressure and smooth muscle cells in rats with pulmonary hypertension. Methods Sixty rats were randomly divided into blank control group, model control group, experimental group and experimental control group, with 15 rats in each group. The model control group, experimental group and experimental control group were established pulmonary hypertension rat model by cannula connection of the right common carotid artery and external jugular vein. The blank control group only performed sham operation to expose the common carotid artery. The adenovirus (Adeno-p53) carrying the wild-type p53 gene was transfected into the experimental group by tracheal aspiration and the recombinant adenovirus vector (Adeno-lacZ) was transfected into the experimental control group with the same method. The virus preservation solution was transfected into the blank control group And model control group. The expression of p53 gene was analyzed by Western blot. Right ventricular mean pressure (mRVP) and mean pulmonary artery pressure (mPAP) were measured by right ventricular catheterization. Morphological changes of pulmonary arterioles were observed by HE staining. (WT%) and AI (Apoptosis Index) were evaluated to evaluate the effect of wild-type p53 gene transfection on pulmonary artery pressure and apoptosis of rat smooth muscle cells. Results After Adeno-p53 was successfully transfected into experimental group, mRVP, mPAP, RVHI and WT% of rats in the experimental group were lower than those in the other three groups (P <0.05). AI in pulmonary artery smooth muscle cells was higher than that in the other three groups (P <0.05). CONCLUSIONS: Adeno-p53 gene transfection can relieve pulmonary hypertension in rats with pulmonary hypertension to some extent. The mechanism may be related to the increased apoptosis of pulmonary artery smooth muscle cells induced by wild-type p53 gene.