Guavinoside B from: Psidium guajava alleviates acetaminophen-induced liver injury via regulating the Nrf2 and JNK signaling pathways
Document Type
Article
Date of Original Version
9-1-2020
Abstract
Benzophenone glycosides are a major type of polyphenols present in guava. To date, there is still poor understanding of the relationship between benzophenone glycosides and the hepatoprotective effects attributed to this edible fruit. Herein, the protective effects of guavinoside B (GUB), a main benzophenone glycoside present in guava fruit, against acetaminophen (APAP)-induced liver injury were investigated in vitro and in vivo. Fluorescence measurement demonstrated that GUB (at a concentration of 30 µM) significantly reduced the intracellular ROS levels in APAP-treated HepG2 cells. In addition, GUB (100 mg kg-1 d-1) pretreatment markedly alleviated APAP-induced hepatocyte infiltration and necrosis in C57BL/6 mice, and improved serum and hepatic biochemical parameters, such as ALT, AST, SOD, GSH, ROS, MDA, and TNF-a levels. RT-PCR and western blot experiments revealed that GUB up-regulated Nrf2, GCLC and NQO1, while reducing p-JNK gene expression in the liver. The fermentation experiment further revealed that the displayed beneficial effects of GUB in vivo might be related to the gut microbial metabolite gallic acid. These promising data suggested that GUB showed potent hepatoprotective effects through regulating the Nrf2 and JNK signaling pathways. Further investigation of the absorption and metabolism of benzophenones would be warranted to promote the utilization of these phenolics as functional food ingredients against oxidative stress-induced chronic diseases.
Publication Title, e.g., Journal
Food and Function
Volume
11
Issue
9
Citation/Publisher Attribution
Li, Yuanyuan, Jialin Xu, Dongli Li, Hang Ma, Yu Mu, Xueshi Huang, and Liya Li. "Guavinoside B from: Psidium guajava alleviates acetaminophen-induced liver injury via regulating the Nrf2 and JNK signaling pathways." Food and Function 11, 9 (2020): 8297-8308. doi: 10.1039/d0fo01338b.