期刊
AMERICAN JOURNAL OF CHINESE MEDICINE
卷 47, 期 8, 页码 1815-1831出版社
WORLD SCIENTIFIC PUBL CO PTE LTD
DOI: 10.1142/S0192415X19500927
关键词
Ginsenoside Rb1; Panax ginseng; Acetaminophen; Hepatotoxicity; Inflammation; MAPK; PI3K/Akt; Signaling Pathways
资金
- National Natural Science Foundation of China [31770378]
- Jilin Science & Technology Development Plan [20180201083YY, 20191102051YY, 20190103092JH]
- program for the Young Top-notch and Innovative Talents of Jilin Agricultural University
Acute liver injury (ALI) induced by acetaminophen (APAP) is the main cause of drug-induced liver injury. Previous reports indicated liver failure could be alleviated by saponins (ginsenosides) from Panax ginseng against APAP-induced inflammatory responses in vivo. However, validation towards ginsenoside Rb1 as a major and marker saponin may protect liver from APAP-induced ALI and its mechanisms are poorly elucidated. In this study, the protective effects and the latent mechanisms of Rb1 action against APAP-induced hepatotoxicity were investigated. Rb1 was administered orally with 10 mg/kg and 20 mg/kg daily for 1 week before a single injection of APAP (250 mg/kg, i.p.) 1 h after the last treatment of Rb1. Serum alanine/aspartate aminotransferases (ALT/AST), liver glutathione (GSH) depletion, as well as the inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), were analyzed to indicate the underlying protective effects of Rb1 against APAP-induced hepatotoxicity with significant inflammatory responses. Histological examination further proved Rb1's protective effects. Importantly, Rb1 mitigated the changes in the phosphorylation of MAPK and PI3K/Akt, as well as its downstream factor NF-kappa B. In conclusion, experimental data clearly demonstrated that Rb1 exhibited a remarkable liver protective effect against APAP-induced ALI, partly through regulating MAPK and PI3K/Akt signaling pathways-mediated inflammatory responses.
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