Effect of Xuanfei Recipe on mTOR/s6k Signal Pathway in Acute Lung Injury Induced by Endotoxin in Rats
投稿时间:2018-04-17  修订日期:2018-05-08
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KeyWord:Acute lung injury  Xuanfei Fang  mTOR  Rps6kb1
余弘吉 上海中医药大学
杨爱东 上海中医药大学
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      Objective To observe the effect of Xuan Fei prescription on mTOR/s6k signaling pathway in rats with acute lung injury induced by endotoxin and to explore its mechanism. Methods 30 male Wistar rats were selected. The animals were randomly divided into normal control group, model control group, Xuan Fei Fang Group (high and low dose group) and dexamethasone group. The tail vein was injected with LPS to prepare ALI model. The levels of inflammatory factors TNF- a, IL-1 beta and IL-6 in bronchoalveolar lavage fluid (BALF) were measured by ELISA method. The expression of mTOR protein was detected by immunohistochemistry, P-mTOR protein expression in lung tissue was measured by Western blot, Rps6kb1 gene expression in alveolar lavage fluid was measured by RT-PCR, and the pathological changes of lung tissue were observed in rats. Results Compared with the normal group, the TNF- alpha, IL-1, IL-6 and Rps6kb1 in the model group increased significantly (P <0.05), the positive area rate of mTOR protein and the expression of p-mTOR protein decreased significantly (P <0.01, P <0.05). The expression of alpha, IL-6 and Rps6kb1 genes decreased significantly (P <0.01, P <0.05), the positive area rate of mTOR protein and the expression of p-mTOR protein increased significantly (P <0.01, P <0.05). HE staining showed that local pulmonary hemorrhage and necrosis were found in the lung tissue of the model group. The small veins of the lungs expanded, the number of white blood cells in the blood vessels increased significantly, and the pulmonary interstitial edema and inflammatory cell infiltration were observed. Compared with the model group, the treatment group showed interstitial pneumonia. Conclusions Xuan Fei Fang has protective effect on acute lung injury induced by endotoxin in rats. Its mechanism may be related to its downregulation of TNF- alpha, IL-6 , Rps6kb1 gene expression, and up regulation of mTOR and P-mTOR protein expression.
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