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| Protective effect of inhibiting inflammasome activation product caspase-1 on acute liver failure in rats |
| WU Yongfeng ZHANG Yulin HUA Wei GUO Caiping |
| Department of Infection Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China |
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Abstract Objective To investigate the protective effect of inhibiting cysteinyl aspartate-specific proteinase (caspase)-1 on acute liver failure (ALF) in rats. Methods A total of 60 healthy male Wistar rats, weighing about 150-180 g, were divided into the control group, the model group and the intervention group by random number table method, with 20 rats in each group. In the control group, serum and liver tissue were collected. In the model group, rats were intraperitoneally injected with 1200 mg/kg D-galactosamine (D-Galn) and 100 g/kg liponolysaccharide (LPS) to construct the ALF model. Serum and liver tissue were collected 24 h after modeling. In the intervention group, rats were injected with 6 mg/kg of thespecific inhibitor of caspase-1, fluoromethylketone by tail vein in the two hours before modeling. The D-GalN and LPS were given to the same dose as the model group during modeling. Serum and liver tissue were collected in the 24 hours after modeling. The liver tissues were observed by HE staining, and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBil) and interleukin (IL) -1β were measured. Results HE staining results indicated that the model was successful. ALT, AST, TBil and IL-1β levels in the model group were higher than those in the control group, the differences were all highly statistically significant (all P ＜ 0.01), and ALT, AST, TBil and IL-1β levels in the intervention group were lower than those in the model group, the differences were all highly statistically significant (all P ＜ 0.01). Conclusion The inflammatory response caused by caspase-1 is one of the important causes of ALF injury and is expected to be a predictor of ALF and a future therapeutic target.
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