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https://ir.cnu.edu.tw/handle/310902800/34414
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| 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 |
| 顯示於類別: | [藥學系(所)] 期刊論文
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