摘要Purpose::Organ damage caused by electric shock has attracted great attention. Some animal investigations and clinical cases have suggested that electric shock can induce liver injury. This study aimed to investigate the potential mechanism of liver injury induced by electric shock.Methods::Healthy male C57BL/6J mice aged 6-8 weeks were romandly divided into 2 groups: control group and electric shock group. Mice in the electric shock group were shocked on the top of the skull with an electric baton (20 kV) for 5 sec, while mice in the control group were exposed to only the acoustic and light stimulation produced by the electric baton. The effect of electric shock on liver function was evaluated by histological and biochemical analysis, and a metabolomics and transcriptomics study was performed to investigate how electric shock might induce liver damage. All data of this study were analyzed using a 2-tailed unpaired Student's t-test in SPSS 22.0 Statistical Package. Results::The electric shock group had significantly higher serum aspartate aminotransferase and alanine aminotransferase levels than the control group ( p < 0.001), and the shock notably caused cytoplasmic swelling and vacuolization, mild inflammatory cell (mainly macrophages and monocytes) infiltration and acute focal necrosis in hepatocytes ( p < 0.001). A total of 47 differential metabolites and 249 differentially expressed genes (DEGs) were detected using metabolomic and transcriptomic analyses. These differential metabolites were significantly enriched in primary bile acid biosynthesis ( p < 0.05). Gene ontology functional analysis of the DEGs revealed that electric shock disturbed a key biological process involved in the inflammatory response in the mouse liver, and a significant number of DEGs were enriched in Kyoto Encyclopedia of Genes and Genomes-identified pathways related to inflammation, such as the interleukin-17, tumor necrosis factor and mitogen-activated protein kinase signalling pathway. Transcriptomic and metabolomic analyses revealed that bile acid metabolism disturbance including up-regulation of the taurochenodesoxycholic acid, chenodeoxycholic acid and taurocholic acid, and down-regulation of chenodeoxycholic acid clycine conjugate may contribute to the electric shock-induced inflammatory response. Conclusion::Electric shock can induce liver inflammatory injury through the interleukin-17, tumor necrosis factor, and mitogen-activated protein kinase signaling pathway, and the bile acid metabolism disturbance including up-regulation of the taurochenodesoxycholic acid, chenodeoxycholic acid and taurocholic acid, and down-regulation of chenodeoxycholic acid clycine conjugate may contribute to inflammatory liver injury following electric shock.

abstractsPurpose::Organ damage caused by electric shock has attracted great attention. Some animal investigations and clinical cases have suggested that electric shock can induce liver injury. This study aimed to investigate the potential mechanism of liver injury induced by electric shock.Methods::Healthy male C57BL/6J mice aged 6-8 weeks were romandly divided into 2 groups: control group and electric shock group. Mice in the electric shock group were shocked on the top of the skull with an electric baton (20 kV) for 5 sec, while mice in the control group were exposed to only the acoustic and light stimulation produced by the electric baton. The effect of electric shock on liver function was evaluated by histological and biochemical analysis, and a metabolomics and transcriptomics study was performed to investigate how electric shock might induce liver damage. All data of this study were analyzed using a 2-tailed unpaired Student's t-test in SPSS 22.0 Statistical Package. Results::The electric shock group had significantly higher serum aspartate aminotransferase and alanine aminotransferase levels than the control group ( p < 0.001), and the shock notably caused cytoplasmic swelling and vacuolization, mild inflammatory cell (mainly macrophages and monocytes) infiltration and acute focal necrosis in hepatocytes ( p < 0.001). A total of 47 differential metabolites and 249 differentially expressed genes (DEGs) were detected using metabolomic and transcriptomic analyses. These differential metabolites were significantly enriched in primary bile acid biosynthesis ( p < 0.05). Gene ontology functional analysis of the DEGs revealed that electric shock disturbed a key biological process involved in the inflammatory response in the mouse liver, and a significant number of DEGs were enriched in Kyoto Encyclopedia of Genes and Genomes-identified pathways related to inflammation, such as the interleukin-17, tumor necrosis factor and mitogen-activated protein kinase signalling pathway. Transcriptomic and metabolomic analyses revealed that bile acid metabolism disturbance including up-regulation of the taurochenodesoxycholic acid, chenodeoxycholic acid and taurocholic acid, and down-regulation of chenodeoxycholic acid clycine conjugate may contribute to the electric shock-induced inflammatory response. Conclusion::Electric shock can induce liver inflammatory injury through the interleukin-17, tumor necrosis factor, and mitogen-activated protein kinase signaling pathway, and the bile acid metabolism disturbance including up-regulation of the taurochenodesoxycholic acid, chenodeoxycholic acid and taurocholic acid, and down-regulation of chenodeoxycholic acid clycine conjugate may contribute to inflammatory liver injury following electric shock.