基础医学与临床 ›› 2017, Vol. 37 ›› Issue (12): 1720-1723.

• 研究论文 • 上一篇    下一篇

藤黄酸减轻脂多糖诱导的小鼠急性肺损伤

王乐,朱亚平,李碧蓉,韩维娜,易德保   

  1. 邵阳学院
  • 收稿日期:2017-09-21 修回日期:2017-10-19 出版日期:2017-12-05 发布日期:2017-11-29
  • 通讯作者: 王乐 E-mail:syyzwangle@163.com
  • 基金资助:
    湖南省教育厅科学研究项目

Gambogic acid attenuates lipopolysaccharide-induced acute lung injury in mice

  • Received:2017-09-21 Revised:2017-10-19 Online:2017-12-05 Published:2017-11-29

摘要: 目的 探讨藤黄酸(GA)对脂多糖(LPS)所致小鼠急性肺损伤的保护作用及其机制。方法 采用尾静脉注射LPS(4 mg/kg)建立小鼠急性肺损伤模型。实验将小鼠随机分为对照组(control组)、模型组(model组) 、藤黄酸组(GA组)和藤黄酸预处理组(GA + LPS 组), 6 h后测定肺湿/干重比值(W/D);检测髓过氧化物酶(MPO)活性;检测肺泡灌洗液(BALF)中蛋白含量和白细胞计数;ELISA 检测肺匀浆中白介素-1β(IL-1β)和肿瘤坏死因子-α (TNF-α)含量。结果 模型组小鼠肺 W/D、MPO活性、BALF中蛋白含量和白细胞数量均增加,肺组织IL-1β和TNF-α 水平升高(均P < 0. 01);藤黄酸预处理可减轻LPS引起的以上指标变化(均P < 0. 05)。结论 GA可减轻LPS诱导的急性肺损伤,其机制可能与降低肺组织IL-1β和TNF-α的含量、抑制中性粒细胞在肺部的聚集和减轻肺部水肿相关。

关键词: 藤黄酸, 脂多糖, 肺损伤, 肿瘤坏死因子-α, 白介素-1β

Abstract: Objective The present study aimed to explored the effects and mechanism of action of gambogic(GA) on lipopolysaccharide(LPS)-induced acute lung injury(ALI) in Kunming mice. Methods ALI model was established by the injection of lipopolysaccharide into the tail vein of mice(4mg/kg, iv). The mice were randomly divided into control group(control), model group(model), GA group(GA), and pretreatment with GA of ALI group(GA+LPS). After six hours, the wet/dry weight ratio (W/D) of the lung , myeloperoxidase (MPO) activity in lung tissue, levels of total proteins and number of white blood cells in bronchoalveolar lavage fluid (BALF) were determined. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured by the enzyme-linked immunosorbent assay methods. Results Compared with control group, the wet/dry weight ratio (W/D) of the lung , MPO activity in lung tissue, levels of total proteins and number of white blood cells in BALF of LPS group obviously increased, in addition the level of lung tissue TNF-α and IL-1β in LPS group were significantly higher(all P<0.01), while in GA pretreatment groups alleviated all the changes in ALI mice. Conclusions GA pre-treatment attenuated LPS-induced ALI, possibly by inhibiting inflammatory cytokines production so as to decrease the recruitment of neutrophils, reduce pulmonary edema.

Key words: Gambogic acid, lipopolysaccharide, acute lung injury, tumor necrosis factor-α, interleukin-1β