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CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway.

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机构: [1]Department of Biotherapy, Department of Geriatrics, Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China. [2]Affilated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China. [3]Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China. [4]Key Laboratory of Cell Homeostasis and Cancer Research of Guangdong Higher Education Institutes, Guangzhou Medical University, Guangzhou 510182, China.
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CD5 molecule like (CD5L), a member of the scavenger receptor cysteine-rich domain superfamily, plays a critical role in immune homeostasis and inflammatory disease. Acetaminophen (APAP) is a safe and effective antipyretic analgesic. However, overdose may cause liver damage or even liver failure. APAP hepatotoxicity is characterized by extensive necrotic cell death and a sterile inflammatory response, in which the role of CD5L remains to be investigated. In this study, we found that the expression of CD5L was increased in the livers of mice after APAP overdose. Furthermore, CD5L deficiency reduced the increase of alanine transaminase (ALT) level, histopathologic lesion area, c-Jun N-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK) phosphorylation level, Transferase-Mediated dUTP Nick End-Labeling positive (TUNEL+) cells proportion, vascular endothelial cell permeability and release of inflammatory cytokines induced by excess APAP. Therefore, our findings reveal that CD5L may be a potential therapeutic target for prevention and treatment of APAP-induced liver injury.© 2021. The Author(s).

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出版当年[2020]版:
大类 | 2 区 医学
小类 | 3 区 细胞生物学
最新[2025]版:
大类 | 2 区 生物学
小类 | 2 区 细胞生物学
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第一作者机构: [1]Department of Biotherapy, Department of Geriatrics, Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
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通讯机构: [1]Department of Biotherapy, Department of Geriatrics, Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China. [3]Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China. [4]Key Laboratory of Cell Homeostasis and Cancer Research of Guangdong Higher Education Institutes, Guangzhou Medical University, Guangzhou 510182, China.
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