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

doi:10.3390/antiox10060897

CNU IR > Pharmacy and Science > Dept. of Pharmacy > Periodical Articles > Item 310902800/34414

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

Title:	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
Authors:	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
Contributors:	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
Keywords:	Sanghuangporus sanghuang paracetamol hepatoprotective MAPK NF-kappa B pathway Keap1/Nrf2/HO-1 pathway CaMKK beta/LKB1/AMPK pathway anti-inflammation
Date:	2021
Issue Date:	2023-11-11 11:50:36 (UTC+8)
Publisher:	MDPI
Abstract:	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.
Relation:	ANTIOXIDANTS-BASEL, v.10, n.6
Appears in Collections:	[Dept. of Pharmacy] Periodical Articles

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