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 60 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 (5.04 g·kg^-1), SMS-M (2.52 g·kg^-1) and SMS-L (1.26 g·kg^-1) doses, and N-acetylcysteine (NAC) (150 mg·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 6-12 h post-exposure, with the most severe damage observed at 6 h post-stress (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 HSP70, alleviating the abnormal accumulation of ATP (P<0.05). Moreover, SMS notably decreased p-mTOR expression and p62 accumulation, activated LKB1 and AMPK phosphorylation, and increased Beclin1 and LC3 expression levels (P<0.05). Heat stress-induced lung injury was most severe at 6 h 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.

Key words: heat stress, Sheng Mai San, lung injury, AMPK-mTOR pathway, autophagy