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Theabrownin Alleviates PCB138-Induced Intestinal Damage by Suppressing Oxidative Stress-Mediated Intestinal
Xiaoyan Ding1, Yuting Zhong1, Zhiyuan Chen1
1State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Department of Gastroenterology in Xiang'an Hospital of Xiamen University, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
None:
2,2',3,4,4',5'-Hexachlorobiphenyl (PCB138) is a persistent organic pollutant with potential intestinal toxicity. Theabrownin (TB) can improve intestinal injury, but its protective effect against PCB138 remains unclear. This study found that 48-week PCB138 exposure induced ileal damage, inflammation, oxidative stress, and necroptosis in mice, which were mitigated by TB intervention. TB alleviated PCB138-induced intestinal damage by suppressing oxidative-stress-mediated intestinal epithelial cell necroptosis. Mechanistically, both TB and N-acetylcysteine (NAC) suppressed PCB138-triggered ROS and subsequent RIPK1/RIPK3/MLKL phosphorylation. The additive effect of NAC combined with necrostatin-1 confirmed ROS as the upstream trigger and RIPK1 as the downstream executor. TB acts similar to NAC, establishing that it prevents necroptosis by scavenging upstream ROS. This study revealed a new mechanism of PCB138-induced intestinal toxicity and identified TB as a potential protective agent against environmentally pollutant-triggered intestinal inflammation.
