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目的:观察芍药苷(Pae)对LPS诱导的小鼠急性肺损伤的影响及其作用机制。方法:雄性BALB/c小鼠随机分为对照组、脂多糖组(LPS)、芍药苷防治组(Pae+LPS)和芍药苷对照组(Pae),予以双蒸水或Pae(20mg/kg)灌胃,1次/d,连续3 d,于实验第3 d灌胃后1 h,腹腔注射生理盐水或LPS(20 mg/kg)。观察各组小鼠肺组织形态学改变并进行肺损伤评分;用Western blotting检测肺组织髓过氧化物酶(MPO)、胞浆型磷脂酶A2(cPLA2)及磷酸化cPLA2的含量。结果:小鼠腹腔注射LPS后12 h,肺组织损伤明显,肺泡间隔增厚,大量炎症细胞浸润,可见明显肺出血及肺水肿;肺组织MPO含量、磷酸化cPLA2水平显著升高。芍药苷防治组与LPS组相比,肺组织损伤明显减轻,炎症细胞浸润减少,肺出血、肺水肿显著减轻;肺MPO含量、磷酸化cPLA2水平明显降低。芍药苷对照组与正常对照组相比,小鼠肺组织结构,MPO含量及磷酸化cPLA2水平未见明显差别。结论:芍药苷通过抑制肺组织中性粒细胞浸润、降低MPO含量和cPLA2活性,减轻小鼠内毒素性肺损伤。
Objective: To observe the effect of paeoniflorin on LPS-induced acute lung injury and its mechanism. Methods: Male BALB / c mice were randomly divided into control group, lipopolysaccharide group (LPS), Pae + LPS group and paeoniflorin control group (Pae), double distilled water or Pae (20mg / kg) The mice were given intragastrically with saline or LPS (20 mg / kg) intraperitoneally 1 h after intragastric administration once a day for 3 days. The morphological changes of the lung tissue of the mice in each group were observed and scored for lung injury. The levels of myeloperoxidase (MPO), cytoplasmic phospholipase A2 (cPLA2) and phosphorylated cPLA2 in lung tissue were detected by Western blotting. RESULTS: At 12 h after intraperitoneal injection of LPS, the lung tissue was damaged and the alveolar septum was thickened. A large number of inflammatory cells infiltrated. Significant pulmonary hemorrhage and pulmonary edema were observed. The levels of MPO and phosphorylated cPLA2 in lung tissue were significantly increased. Paeoniflorin control group compared with LPS group, lung tissue injury was significantly reduced, inflammatory cell infiltration decreased, pulmonary hemorrhage, pulmonary edema significantly reduced; pulmonary MPO levels, phosphorylated cPLA2 levels were significantly lower. Paeoniflorin control group compared with the normal control group, the mouse lung tissue structure, MPO content and phosphorylated cPLA2 levels no significant difference. Conclusion: Paeoniflorin can reduce endotoxin-induced lung injury in mice by inhibiting neutrophil infiltration, decreasing MPO content and cPLA2 activity.