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• W4379095018 abstract "The early stages of brain injury can induce acute liver injury, which can be recovered in the short term. Continued medication treatment during hospitalization for brain injury alleviates the prognosis and contributes to a high incidence of drug-induced liver injury (DILI). We hypothesize that there is an interaction between changes in the hepatic environment after brain injury and liver injury produced by intensive drug administration, leading to an upregulation of the organism's sensitivity to DILI. In this study, mice models of TBI were established by controlled cortical impact and models of DILI were constructed by acetaminophen (APAP). All mice were divided into four groups: Sham, TBI, APAP, and TBI+APAP, and related liver injury indicators in liver and serum were detected by Western blot, RT-PCR, and immunohistochemical staining. The results suggested that liver injury induced in the early stages of brain injury recovered in three days, but this state could still significantly aggravate DILI, represented by higher liver enzymes (AST and ALT), oxidative stress (increase in malondialdehyde concentration and deregulation of glutathione and superoxide dismutase activities), inflammatory response (activation of HMGB1/TLR4/NF-κB signaling pathway, and increased mRNA and protein levels of pro-inflammatory cytokines including TNF-α, IL-6, and IL-1β), and apoptosis (TUNEL assay, upregulation of Bax protein and deregulation of Bcl-2 protein). In summary, our results suggested that traumatic brain injury is a potential susceptibility factor for DILI and exacerbates DILI." @default.
• W4379095018 created "2023-06-03" @default.
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• W4379095018 date "2023-06-02" @default.
• W4379095018 modified "2023-10-14" @default.
• W4379095018 title "Susceptibility to Hepatotoxic Drug-induced Liver Injury Increased after Traumatic Brain Injury in Mice" @default.
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• W4379095018 doi "https://doi.org/10.1089/neu.2022.0147" @default.
• W4379095018 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37265124" @default.
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