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目的:考察芪白平肺颗粒对野百合碱诱导致肺动脉高压大鼠的治疗作用及可能机制。方法:采用腹腔注射野百合碱50 mg/kg建立模型,造模后第3天开始分组给药,组别分别为芪白平肺颗粒组(4.4、2.2、1.1 g生药/kg),阳性对照组(硝苯地平8mg/kg),对照组与模型组灌胃给予等量溶媒,每天1次,连续4周。第29天灌胃给药后检测肺动脉压力及右心室压力,计算右心指数,测定血浆NO、ET-1水平,匀浆肺组织测定TNF-α及IL-6含量,并对右心室及肺组织进行病理检测。结果:与模型组相比,芪白平肺颗粒2.2、4.4 g生药/kg组大鼠肺动脉压力及右心室压力显著降低,血浆NO升高,ET-1降低,芪白平肺颗粒2.2、4.4 g生药/kg组大鼠右心指数显著减小,病理损伤均有不同程度的缓解或改善,肺小动脉血管壁厚度系数及面积系数显著降低,以4.4 g生药/kg效果最佳。结论:芪白平肺颗粒可降低肺动脉高压,减轻右心室肥厚,减轻心肺组织病理变化,平衡内皮细胞功能,减轻炎症损伤,缓解肺血管重塑为其缓解肺动脉高压,延缓慢性阻塞性肺疾病的可能机制之一。
Objective: To investigate the therapeutic effect of Qibai Pingfei granule on monocrotaline-induced pulmonary hypertension in rats and its possible mechanism. Methods: The model was established by intraperitoneal injection of monocrotaline (50 mg / kg). The rats were administered with Qibai Pingfei Granules (4.4,2.2,1.1 g crude drug / kg), and the positive control Group (nifedipine 8mg / kg). The control group and model group were intragastrically given the same amount of vehicle once a day for 4 weeks. On day 29, pulmonary artery pressure and right ventricular pressure were measured after intragastric administration, and the right heart index was calculated. Plasma NO and ET-1 levels were measured. Homogenate lung tissue was measured for TNF-α and IL-6 levels. Tissue for pathological examination. Results: Compared with the model group, the pulmonary arterial pressure and right ventricular pressure of rats in 2.2, 4.4 g crude drug / kg group of Qibai Pingfei granule were significantly decreased, NO in plasma increased, ET-1 decreased, g crude drug / kg group, the right heart index was significantly reduced, the pathological changes were alleviated or improved to varying degrees, pulmonary arteriole wall thickness coefficient and area coefficient decreased significantly to 4.4 g crude drug / kg the best. Conclusion: Qibai Pingfei Granules can reduce pulmonary hypertension, reduce right ventricular hypertrophy, reduce the pathological changes of heart and lung tissue, balance the function of endothelial cells, reduce inflammation, relieve pulmonary vascular remodeling to relieve pulmonary hypertension and delay chronic obstructive pulmonary disease One of the possible mechanisms.