• Shen Ren, Jing Leng, Xing-Yue Xu, Shuang Jiang, Ying-Ping Wang, Xiao-Tong Yan, Zhi Liu, Chen Chen, Zi Wang, and Wei Li.
• College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, P. R. China.
• Am. J. Chin. Med. 2019 Jan 1; 47 (8): 1815-1831.

AbstractAcute 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- α (TNF- α ), interleukin-1 β (IL-1 β ), 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- κ 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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