Hepatoprotective effects of chlorogenic acid on mice exposed to aflatoxin B1: Modulation of oxidative stress and inflammation.

Aflatoxin B1 (AFB1) is widely distributed in crops and feeds, and ingestion of AFB1-contaminated crops is harmful to human/animal health. This study was designed to investigate hepatoprotective effects of chlorogenic acid (CGA), due to its excellent antioxidant and anti-inflammatory activities, on mice exposed to AFB1. Male Kunming mice were orally fed with CGA prior to daily AFB1 exposure for 18 consecutive days. The results showed that CGA treatment reduced the serum activity of aspartate aminotransferase, hepatic malondialdehyde content and pro-inflammatory cytokines synthesis, prevented histopathological changes of the liver, increased hepatic glutathione level, catalase activity and IL10 mRNA expression in mice subjected to AFB1. Taken together, CGA exerted the protective effect on AFB1-induced hepatic damage by modulating redox status and inflammation, suggesting that CGA may be a candidate compound for the treatment of aflatoxicosis.

Aflatoxin-B1-Exposure-Induced Hepatic Injury Could Be Alleviated by Polydatin through Reducing Oxidative Stress, Inhibiting Inflammation and Improving Mitophagy.

Aflatoxin B1 (AFB1) is a toxic food/feed pollutant, exerting extensive deleterious impacts on the liver. Oxidative stress and inflammation are considered to be vital contributors to AFB1 hepatotoxicity. Polydatin (PD), a naturally occurring polyphenol, has been demonstrated to protect and/or treat liver disorders caused by various factors through its antioxidant and anti-inflammatory properties. However, the role of PD in AFB1-induced liver injury is still elusive. Therefore, this study was designed to investigate the protective effect of PD on hepatic injury in mice subjected to AFB1. Male mice were randomly divided into three groups: control, AFB1 and AFB1-PD groups. The results showed that PD protected against AFB1-induced hepatic injury demonstrated by the reduced serum transaminase activity, the restored hepatic histology and ultrastructure, which could be attributed to the enhanced glutathione level, the reduced interleukin 1 beta and tumor necrosis factor alpha concentrations, the increased interleukin 10 expression at transcriptional level and the up-regulated mRNA expression related to mitophagy. In conclusion, PD could alleviate AFB1-induced hepatic injury by reducing oxidative stress, inhibiting inflammation and improving mitophagy.