The Role of Key Molecules of Pyroptosis in Liver Damage of Rats With Exertional Heat Stroke.

This study is aimed at investigating the role of key molecular elements involved in pyroptosis in liver injury caused by exertional heat stroke (EHS). We established a model of EHS-induced liver injury in Sprague-Dawley rats, with a control group (receiving no treatment) for comparison and 12 rats in each group. Alanine transaminase (ALT) and aspartate transaminase (AST) levels in the blood were detected. Interleukin-1 beta (IL-1) and interleukin-18 (IL-18) levels were assessed using enzyme-linked immunosorbent assays (ELISA). Pathological changes in liver tissue were examined by hematoxylin and eosin (H&E) staining. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to detect mRNA and protein expression levels of Caspase-1 and Gasdermin D. Compared to the control group, the liver tissue of the EHS group showed congestion in hepatic sinusoids, hepatocyte edema, eosinophilic changes, necrosis, and infiltration of inflammatory cells. ALT and AST levels in the EHS group were significantly higher than those in the control group ( < 0.05). The mRNA expressions of Caspase-1, Gasdermin D, IL-1, and IL-18 were significantly increased in the EHS group compared to the control group ( < 0.001). The protein expressions of Caspase-1, cleaved Caspase-1, Gasdermin D, and cleaved Gasdermin D were significantly increased in the EHS group. These findings indicated that hepatic pyroptosis plays an important role in EHS-induced liver injury.