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    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34414


    標題: Sanghuangporus sanghuang Mycelium Prevents Paracetamol-Induced Hepatotoxicity through Regulating the MAPK/NF-kappa B, Keap1/Nrf2/HO-1, TLR4/PI3K/Akt, and CaMKK beta/LKB1/AMPK Pathways and Suppressing Oxidative Stress and Inflammation
    作者: Jiang, Wen-Ping
    Deng, Jeng-Shyan
    Huang, Shyh-Shyun
    Wu, Sheng-Hua
    Chen, Chin-Chu
    Liao, Jung-Chun
    Chen, Hung-Yi
    Lin, Hui-Yi
    Huang, Guan-Jhong
    貢獻者: China Med Univ, Dept Chinese Pharmaceut Sci & Chinese Med Resourc, Coll Chinese Med
    Chia Nan Univ Pharm & Sci, Dept Pharm
    Asia Univ, Dept Occupat Therapy
    Asia Univ, Dept Hlth & Nutr Biotechnol
    China Med Univ, Sch Pharm
    Natl Museum Nat Sci, Dept Biol
    Grape King Biotechnol Ctr
    關鍵字: Sanghuangporus sanghuang
    paracetamol
    hepatoprotective
    MAPK
    NF-kappa B pathway
    Keap1/Nrf2/HO-1 pathway
    CaMKK beta/LKB1/AMPK pathway
    anti-inflammation
    日期: 2021
    上傳時間: 2023-11-11 11:50:36 (UTC+8)
    出版者: MDPI
    摘要: Liver damage induced by paracetamol overdose is the main cause of acute liver failure worldwide. In order to study the hepatoprotective effect of Sanghuangporus sanghuang mycelium (SS) on paracetamol-induced liver injury, SS was administered orally every day for 6 days in mice before paracetamol treatment. SS decreased serum aminotransferase activities and the lipid profiles, protecting against paracetamol hepatotoxicity in mice. Furthermore, SS inhibited the lipid peroxidation marker malondialdehyde (MDA), hepatic cytochrome P450 2E1 (CYP2E1), and the histopathological changes in the liver and decreased inflammatory activity by inhibiting the production of proinflammatory cytokines in paracetamol-induced acute liver failure. Moreover, SS improved the levels of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase in the liver. Significantly, SS diminished mitogen-activated protein kinase (MAPK), Toll-like receptor 4 (TLR4), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), and the nuclear factor-kappa B (NF-kappa B) axis, as well as upregulated the Kelch-like ECH-associated protein 1 (Keap1)/erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, in paracetamol-induced mice. SS mainly inhibited the phosphorylation of the liver kinase B1 (LKB1), Ca2+/calmodulin-dependent kinase kinase beta (CaMKK beta), and AMP-activated protein kinase (AMPK) protein expression. Furthermore, the protective effects of SS on paracetamol-induced hepatotoxicity were abolished by compound C, an AMPK inhibitor. In summary, we provide novel molecular evidence that SS protects liver cells from paracetamol-induced hepatotoxicity by inhibiting oxidative stress and inflammation.
    關聯: ANTIOXIDANTS-BASEL, v.10, n.6
    Appears in Collections:[藥學系(所)] 期刊論文

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