生脉散对热应激大鼠肺脏AMPK-mTOR通路及自噬的影响

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中图分类号：S853.74 文献标志码：A 文章编号：0366-6964（2025）10-5277-12

Abstract： This study aims to investigate the occurrence of heat stress and the therapeutic effects and mechanisms of Sheng Mai San （SMS） in treating heat stress-induced lung injury，providing theoretical support for the application of SMS in this context. Forty-eight SD rats were selected to establish heat stress models based on the recovery time of heat stress. Another 6O SD male rats were randomly divided into 6 groups （ n=10 per group）. Each group was given intragastradized administration 2 hours before heat stress every day，and the Control group and heat stress group （HS） were given normal saline. SMS group was administered at SMS-H （2 （5.04g⋅kg-1） ），SMS-M （2.52g⋅kg-1 ）and SMS-L （1.26g∙kg-1 ） doses，and N-acetylcysteine（NAC） （150mg⋅kg-1 ） was set up as a positive control group. Sampling was performed after the end of heat stress on day 7. Biological techniques including HE staining，Masson staining，Western blot，and real-time quantitative PCR were employed to evaluate the effects of SMS on heat stress-induced lung injury and its potential mechanisms. Heat stress caused significant lung injury between 6-12h post-exposure，with the most severe damage observed at 6h poststress（ P<0.05） .Real-time quantitative PCR，Western blot，and biochemical analyses revealed that SMS significantly reduced the expression levels of inflammatory cytokines TNF-α ， IL-1β IL-10，IL-6，and HSP7o，alleviating the abnormal accumulation of ATP （ P<0.05 ）.Moreover， SMS notably decreased p-mTOR expresson and p62 accumulation， activated LKBl and AMPK phosphorylation，and increased Beclinl and LC3 expression levels （ P<0. 05. ）. Heat stress-induced lung injury was most severe at 6h post-exposure. SMS demonstrated therapeutic effects by activating the AMPK-mTOR pathway， promoting autophagy，and clearing damaged lung cells， thereby mitigating heat stress-induced lung injury.

Keywords： heat stress; Sheng Mai San; lung injury； AMPK-mTOR pathway； autophagy∗ Corresponding author： WEI Yanming，E-mail： weiym@gsau. edu. cn

动物在高温高湿环境下超过了机体的承受能力而产生非特异性反应的综合征称为热应激（heatstress，HS）[1]。（剩余17049字）