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目的研究angiopoietin家族成员在高动力型肺动脉高压形成中的作用。方法通过左颈总动脉和左颈外静脉分流手术建立大鼠高动力型肺动脉高压模型。术后第1、2、4、8和12周检测肺组织内Ang-1、Ang-2、Ang-3、Tie2和激活型caspase-3的变化。结果高动力引起肺动脉高压,出现肺动脉内皮细胞增生肥大。在肺动脉高压形成的过程中,肺组织内Ang-1和Tie2的表达显著增高,而Ang-3的表达明显降低。肺微小动脉内皮细胞Tie2的磷酸化水平逐渐升高但激活型caspase-3却降低。Ang-2的表达未见明显变化。结论内皮细胞凋亡减少可能是高动力型肺动脉高压形成的一个重要的病理机制。Ang-1/Tie2可能通过抑制内皮细胞凋亡来促进高动力型肺动脉高压的形成。Ang-3的表达量下降可能也促进了这一过程。在高动力型肺动脉高压的形成过程中Ang-2可能不发挥作用。
Objective To investigate the role of angiopoietin family members in the formation of high-powered pulmonary hypertension. Methods High-powered pulmonary hypertension model was established by shunting left common carotid artery and left external jugular vein. The changes of Ang-1, Ang-2, Ang-3, Tie2 and activated caspase-3 in lung tissue were detected at 1, 2, 4, 8 and 12 weeks after operation. The results of high power pulmonary hypertension caused by pulmonary hypertrophy of endothelial cell proliferation. In the process of pulmonary hypertension, the expression of Ang-1 and Tie2 in lung tissue was significantly increased, while the expression of Ang-3 was significantly decreased. Phosphorylation of Tie2 in pulmonary arteriolar endothelial cells gradually increased but active caspase-3 decreased. Ang-2 expression no significant change. Conclusion The decrease of apoptosis of endothelial cells may be an important pathological mechanism of the formation of hyperactive pulmonary hypertension. Ang-1 / Tie2 may promote the formation of hyperkinetic pulmonary hypertension by inhibiting endothelial cell apoptosis. The decrease in Ang-3 expression may also contribute to this process. Ang-2 may not play a role in the formation of hyperactive pulmonary hypertension.