Sulforaphane Alleviates Bisphenol A-Induced Glucose Intolerance via Improving Inflammation and Oxidative Stress

Abstract

Background. Bisphenol A (BPA) disrupts glucose homeostasis via inflammatory pathways in liver cells, affecting insulin sensitivity. This study examines sulforaphane (SFN), known for its anti-inflammatory and antioxidative properties, for counteracting BPA’s effects. Methods. We evaluated SFN’s impact on BPA-exposed C57/BL6J mice and HepG2 cells, focusing on metabolic parameters, insulin signaling, and inflammatory markers. Mice were treated with SFN (10 mg/kg) for six weeks, with assessments including body weight, serum glucose, insulin levels, and glucose tolerance. Molecular analyses in both models included gene expressions related to glucose metabolism, insulin and MAPK signaling pathways, and markers of inflammation and oxidative stress. Results. SFN reduced blood glucose and improved glucose tolerance of BPA-treated mice. In BPA-treated HepG2 cells, SFN significantly boosted glucose consumption in vitro. Moreover, SFN treatment enhanced the protein expression of phosphorylated-insulin receptor and phosphorylated-AKT and reversed glycolytic and gluconeogenic gene expression in HepG2 cells and mice liver. SFN also decreased phosphorylation levels of p38 and JNK and reduced inflammation and oxidative stress markers in vitro and in vivo. Conclusion. Our findings underscore SFN’s capacity to ameliorate BPA-induced glucose intolerance and insulin resistance by enhancing hepatic insulin signaling and metabolic functions. This action is likely mediated through SFN’s inhibitory effects on inflammatory and oxidative pathways. Consequently, SFN holds promise as an intervention for mitigating BPA-related metabolic disorders.