2. Academic Validation
  3. Capsaicin alleviates acetaminophen-induced acute liver injury in mice

Capsaicin alleviates acetaminophen-induced acute liver injury in mice

  • Clin Immunol. 2020 Nov;220:108578. doi: 10.1016/j.clim.2020.108578.
Xiang Zhan 1,  Jianqiang Zhang 2,  Hui Chen 1,  Liyuan Liu 1,  Yiming Zhou 1,  Ting Zheng 1,  Suxiao Li 1,  Yanxiang Zhang 1,  Bing Zheng 3,  Quan Gong 4
Affiliations

Affiliations

  • 1 Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China.
  • 2 Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China; Department of Nephrology, Ezhou Central Hospital, Ezhou, China.
  • 3 Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China; Clinical Molecular Immunology Center, School of Medicine, Yangtze University, Jingzhou, China. Electronic address: hxzheng@yangtzeu.edu.cn.
  • 4 Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China; Clinical Molecular Immunology Center, School of Medicine, Yangtze University, Jingzhou, China. Electronic address: gongquan1998@163.com.
PMID: 32861810 DOI: 10.1016/j.clim.2020.108578
Abstract

Overdose of N-acetyl-para-aminophenol (APAP) can induce acute liver injury (ALI). We evaluated the potential protective effect of 8-methyl-N-geranyl-6-nonamide (capsaicin (CAP)) in APAP-induced ALI in mice. ALI was induced by APAP (150 mg/kg, i.p.) administration; CAP pretreatment (1 mg/kg) was undertaken before APAP injection for 3 consecutive days. We found that CAP pretreatment attenuated ALI significantly; improve the oxidative stress-associated Indicators (hepatic expression of malondialdehyde (MDA) superoxide dismutase (SOD) and glutathione (GSH)); downregulate expression of proinflammatory cytokines (interleukin (IL)-6, IL-1β, tumor necrosis factor-α) through the high-mobility group box 1/toll-like receptor-4/nuclear factor-kappa B (HMGB1/TLR4/NF-κB) signaling pathway; alleviate hepatocyte Apoptosis by inhibiting expression of B-cell lymphoma-2-associated X, Caspase-3 and cleaved Caspase-3. CAP pretreatment reduced expression of B-cell lymphoma-2, which served as a hepatotoxic factor rather than an anti-apoptotic protein in our mouse model. We propose that CAP can alleviate APAP-induced ALI by inhibiting the inflammatory response, attenuating oxidative stress, and reducing hepatocyte Apoptosis.

Keywords

Acetaminophen; Acute liver injury; Apoptosis; Capsaicin; HMGB1/TLR4/NF-κB signaling pathway; Inflammation.

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