Abstract: Objective To investigate the effect of Shegan Zhike Capsule on lipopolysaccharide ( LPS) - induced acute lung injury (ALI) in rats. Method 70 rats were randomly divided into 7 groups according to their body weights, namely, blank group, model group, low, medium and high dose groups of Shegan Zhike capsule (30. 00 mg, 60. 00 mg,120. 00 mg extract / kg) ,Zhongyang and Xiyang groups, with 10 rats in each group. They were administered for 7 consecutive days. On the fifth day of the experiment, 1 h after the administration by gavage, except for the blank group, rats in other groups were instilled with LPS (5 mg / kg) intratracheally to make Ali rat models, The blank control group was infused with the same dose of normal saline. 48 hours after model establishment, blood was collected from abdominal aorta of rats to measure IL-1β、TNF-α content. The whole lung was taken and weighed to calculate the lung index. The left lung tissue of rats was taken to measure the wet / dry mass ratio of the lung. The right middle lobe of lung was taken for pathological observation. Result Compared with the model control group, The contents of IL-1β and TNF-αin the low, medium and high dose groups ( 30. 00 mg, 60. 00 mg, 120. 00 mg extract / kg) of Shegan Zhike capsule were significantly decreased (P<0. 01) ; Compared with the model control group, the lung index and lung wet / dry mass ratio of rats in the high dose group of Shegan Zhike capsule were significantly reduced ( P< 0. 01,P< 0. 05) ;Compared with the blank control group, the alveolar space of the model control group was widened, the alveolar cavity exudation, and the degree of alveolar damage and destruction were significantly increased ( P<0. 01,P<0. 05) . Conclusion Shegan Zhike capsule has a protective effect on lipopolysaccharide induced acute lung injury in rats, and its mechanism may be related to reducing pulmonary edema and inhibiting the synthesis and release of inflammatory factors.

Key words: acute lung injury, inflammatory factors, rat

摘要： 目的 探讨射干止咳胶囊对脂多糖( LPS)致急性肺损伤( ALI) 大鼠的影响。 方法 选择 70 只大鼠,按体质量随机分为 7 组,即空白组、模型组、射干止咳胶囊低、中、高剂量组(30. 00 mg、60. 00 mg、120. 00 mg 提取物 / kg) 、中阳及西阳组,每组 10 只,连续给药 7 d,实验第 5 天灌胃给药后 1 h,除空白组外,将其他各组大鼠气管内滴注 LPS( 5 mg / kg)制作 ALI 大鼠模型,空白对照组滴注相同剂量 0. 9%氯化钠溶液。 造模 48 h 后大鼠腹主动脉采血测定血清中 IL-1β、TNF-α 含量。 取全肺,称重计算肺指数,取大鼠左肺组织测肺湿 / 干质量比,取右肺中叶组织进行病理观察。 结果 与模型对照组比较,射干止咳胶囊低、中、高剂量组( 30. 00 mg、60. 00 mg、120. 00 mg 提取物 / kg) IL-1β、TNF-α 含量明显减少,差异有统计学意义( P< 0. 01) ;与模型对照组比较,射干止咳胶囊高剂量组大鼠肺指数、大鼠肺湿 / 干质量比明显减少,差异有统计学意义(P< 0. 01,P< 0. 05) ;与空白对照组比较,模型对照组大鼠肺泡间隔增宽、肺泡腔内渗出、肺泡损伤破坏程度明显增加,差异有统计学意义(P<0. 01,P<0. 05) 。 结论 射干止咳胶囊对脂多糖诱导大鼠急性肺损伤具有一定的保护作用,其作用机制可能与减轻肺水肿及抑制炎性因子合成释放有关。

关键词: 急性肺损伤, 炎性因子, 大鼠