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Nrf2/HO-1 Dysregulation is Involved in the Microplastic-Induced Gut–Liver Axis Damage Mechanism and the Protective Effect of Astaxanthin
Original title: Nrf2/HO-1 Dysregulation is Involved in the Microplastic-Induced Gut–Liver Axis Damage Mechanism and the Protective Effect of Astaxanthin
Summary
Microplastics found in chicken (a food many of us eat regularly) were shown to damage liver health and disrupt gut bacteria in this animal study, raising concerns about how these plastic particles might affect people through the food chain. The good news: astaxanthin, an antioxidant found in salmon and shrimp, helped protect the liver and gut by boosting the body's natural defense systems—suggesting a possible dietary strategy to counter microplastic-related harm, though more research in humans is needed.
As one of the most consumed meat products globally, microplastics (MPs) residues in chickens may enter the human body through the food chain. Therefore, this study aimed to investigate the adverse effects of MPs exposure on chicken health and the detoxification mechanisms of astaxanthin (AST). We found that MPs significantly impaired liver function, inducing injury characterized by hepatocyte ferroptosis, inflammation, lipid disorder, and fibrosis. This hepatic damage was linked to MPs-induced gut microbiota dysbiosis and disruption of the intestinal barrier. AST exerted hepatoprotective effects by activating the Nrf2/HO-1 signaling pathway and attenuating hepatic oxidative stress and ferroptosis. In parallel, AST improved gut microbiota composition and intestinal barrier integrity, thereby potentially reducing gut-derived inflammatory burden. Together, these findings suggest that AST confers liver protection through both direct hepatic actions and indirect modulation of the gut-liver axis.