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Galangin mitigates polystyrene microplastic-induced hepatotoxicity: modulation of mitochondrial biogenesis, NLRP3 inflammasome, and intrinsic apoptotic signaling
Summary
Microplastics from everyday plastic waste can damage the liver by triggering inflammation, cell death, and stress on cell "batteries" (mitochondria). This rat study found that galangin, a natural compound found in foods like ginger and honey, helped protect the liver from this microplastic-related damage by calming inflammation and boosting the liver's own protective defenses. While these results are promising and point to a possible future remedy for microplastic exposure, this was an animal study, so more research is needed before we know if it works the same way in humans.
BACKGROUND: Polystyrene microplastic (polystyrene) has emerged as a prevalent environmental contaminant that exerts significant hepatic injury. The current work explored the mitigating capability of galangin against polystyrene-evoked hepatotoxicity and unveiled the potential associating molecular pathways. METHODS AND RESULTS: Male Wistar rats (n = 40 in total) were subjected to polystyrene with or without concomitant administration of galangin. Hepatic function, tissue architecture, and key molecular signaling pathways were evaluated using ELISA, histopathological examinations, and Western blotting techniques. Galangin co-administration was associated with mitigation of hepatic dysfunction and tissue damage, as evidenced by a significant decrease of serum bilirubin and amelioration of the histopathological alterations. Additionally, hepatic inflammation was reduced, as indicated by modulation of the inflammatory cytokines. Moreover, hepatocellular apoptosis and oxidative stress were suppressed. At the molecular level, galangin co-administration was accompanied by suppression of NF-κB and NLRP3 inflammatory signaling, upregulation of the Nrf2/NQO1 antioxidant axis, and inhibition of p53 apoptotic signaling. In addition, mitochondrial biogenesis was enhanced, as indicated by upregulation of SIRT1/Tfam axis. CONCLUSIONS: These findings provide the first evidence introducing galangin as a potential intervention against the polystyrene-evoked hepatotoxicity and unveiling the associating molecular changes. These changes involve the concurrent suppression of inflammation, oxidative stress, apoptosis, alongside the improvement of mitochondrial biogenesis.