芪白平肺颗粒对肺动脉高压大鼠的影响及机制研究

Effect and mechanism of Qibaipingfei granules on monocrotaline-induced pulmonary hypertension in rats

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 effect of Qibaipingfei granules on monocrotaline-induced pulmonary hypertension in rats and determine it’s mechanism. Methods： The rat model was established by monocrotaline（ MCT） in traperitoneal injection of 50 mg / kg. All rats were treated with medicine once a day for four weeks after modeling three days,except that normal and model group were given the same amount of solvent. SD rats were randomly divided into 6 groups,other group were QBPF granules groups（ 4. 4,2. 2,1. 1 g / kg） and nifedipine group. On day 29,mean pulmonary artery pressure（ m PAP） and mean right ventricle pressure（ mRVP） were mesured,the index of right ventricular hypertrophy（ RVHI） was calculated,the ET-1 and NO content in blood plasma,level of TNF-α and IL-6 in lung tissue were measured,histopathologic changes in lung and right ventricle was observed. Results： Compared with model group,the m PAP and mRVP were significantly decreased in QBPF 1. 1,2. 2,4. 4 g / kg groups and nifedipine group. Plasma levels of ET-1 was decreased and levels of NO were significantly increased in QBPF 2. 2,4. 4 g / kg groups,RVHI was decreased and the pathological changes of lung tissue and right ventricle were improved by QBPF granules. Conclusion： QBPF granules can reduce pulmonary arterial pressure,antagonize right ventricle thickness,and improve pathological changes of lung tissue and right ventricle. Balancing endothelial function and remitting vascular remodeling may be important mechanisms for reducing pulmonary arterial pressure and treating chronic obstructive pulmonary disease.