实验动物科学

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参附注射液对内毒素休克大鼠肺组织表达PPARγ和TNFα的干预作用

    

  1. 贵州中医药大学基础医学院,贵州中医药大学第二临床医学院
  • 出版日期:2020-10-28 发布日期:2021-02-25

Effect of Shenfu Injection on the Expression of PPARγ and TNFα in Lung Tissue of Rats with Endotoxic Shock

    

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  • Online:2020-10-28 Published:2021-02-25
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摘要: 摘要:目的 观察内毒素休克大鼠肺组织中过氧化物酶体增殖物激活受体γ(PPARγ)和肿瘤坏死因子α(TNFα)的表达情况及参附注射液的干预作用。方法 经腹腔注射脂多糖(LPS)建立内毒素休克SD大鼠模型,用低、中、高剂量参附注射液进行治疗,观察肺组织病L改变,检测肺组织中PPARγ和TNFα的表达量,同时检测血浆中TNFα和IL-1β的水平。结果 模型组大鼠具有典型的急性肺损伤表现;肺组织中PPARγ的转录和表达(P<0.01)量均显著下调,TNFα的表达明显增加(P<0.01);血浆中TNFα和IL-1β水平明显上升(P<0.01)。与模型组比较,参附注射液改善肺组织充血、水肿及炎性细胞浸润;呈剂量依赖性上调肺组织中PPARγ的转录和表达,下调TNFα的表达;同时抑制血浆中炎症介质TNFα和IL-1β水平(P<0.01)。结论 参附注射液保护内毒素休克大鼠肺组织,其作用机制可能与上调PPARγ从而抑制炎症介质的产生有关。

 

Abstract: Abstract: Objective To investigate expression of peroxisome proliferator activated receptor gamma ( PPARγ) and tumor necrosis factor alpha ( TNFα) in lung tissue of rats with endotoxic shock and the intervention effect of Shenfu injection. Method SD rats were selected to establish the animal model of endotoxin shock by intraperitoneal injection of lipopolysaccharide ( LPS ) , followed by the treatment with shenfu injection ( low, medium and high doses) . The pathological changes of lung tissue were observed. The transcription and expression of PPARγ and TNFα in lung tissue and secretion of TNFα and IL-1β in plasma were detected. Result There were typical acute lung injury in the rats of LPS group, the transcription and expression of PPARγ in lung tissue were significantly decreased ( P<0. 01) , the expression of TNFα was obviously increased ( P < 0. 01) , and the levels of TNFα and IL-1β in plasma were significantly increased ( P < 0. 01) . However, compared with LPS group, Shenfu Injection relieved pulmonary congestion, edema and inflammatory cell infiltration, increased the transcription and expression of PPARγ in lung tissue in a dose-dependent manner, decreased TNFα expression, and inhibited the levels of inflammatory factors TNFα and IL-1β in plasma as well ( P < 0. 01) . Conclusion Shenfu injection can protect lung tissue of rats with endotoxic shock, and its mechanism may be related to up regulating PPARγ and inhibiting the production of inflammatory mediators.