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目的研究染料木黄酮对大鼠慢性栓塞性肺动脉高压(Chronic thromboembolic pulmonary hypertension,CTEPH)的减缓作用及对肺组织一氧化氮合酶(Endothelial nitric oxide synthase,eNOS)水平的影响,并探讨其可能的机制。方法雄性SD大鼠麻醉后,经颈静脉回输体外制备的自体血栓栓子,2周后同法进行二次栓塞,将造模成功的大鼠分为染料木黄酮治疗组、栓塞4周组和8周组。全程腹腔注射抗纤维溶解剂氨甲环酸,达目标日期后,采用右心导管法检测平均肺动脉压;开胸取心肺组织,心脏左右心室、室间隔分别称重后,计算右心室肥厚指数,电镜下观察肺小动脉结构变化;Western blot法检测肺组织中eNOS水平。结果染料木黄酮治疗组及栓塞8周组大鼠平均肺动脉压及右心室肥厚指数较栓塞4周组明显升高(P均<0.01),染料木黄酮组较栓塞8周组显著降低(P<0.01);染料木黄酮治疗组及栓塞8周组大鼠肺小动脉结构重塑(平滑肌细胞明显增殖);染料木黄酮治疗组大鼠肺组织中eNOS水平较栓塞4周和8周组明显升高(P<0.01)。结论染料木黄酮能减缓大鼠慢性栓塞性肺动脉高压的进展,其机制可能与其上调eNOS的水平有关。
Objective To study the effect of genistein on slowing of chronic embolic pulmonary hypertension (CTEPH) and its effect on lung tissue nitric oxide synthase (eNOS) mechanism. Methods Male Sprague-Dawley rats were anesthetized and transfused with autologous thrombus in vitro. Two weeks later, they were re-embolized. The rats were divided into genistein group and 4-week group And 8 weeks group. Intraperitoneal injection of anti-fibrinolytic agent tranexamic acid, the target date, the right heart catheterization was used to detect the mean pulmonary arterial pressure; chest open heart and lung tissue, left and right ventricles of the heart and ventricular septum were weighed, calculate the right ventricular hypertrophy index, The structure of pulmonary arterioles was observed under electron microscope. The eNOS level in lung tissue was detected by Western blot. Results The mean pulmonary arterial pressure and right ventricular hypertrophy index in genistein group and the 8-week embolization group were significantly higher than those in the 4-week embolization group (all P <0.01), and the genistein group was significantly lower than the 8-week embolization group (P < 0.01). The structure remodeling of pulmonary arterioles was observed in the genistein treated group and the 8-week embolization group (the proliferation of smooth muscle cells was significant). The eNOS level in the lung tissue of the genistein-treated group was significantly higher than that of the 4 and 8-week embolization High (P <0.01). Conclusion Genistein can slow down the progression of chronic embolic pulmonary hypertension in rats, which may be related to its up-regulation of eNOS.