Coconut Haustorium Alleviates Fructose-Induced Redox Imbalance, Lipotoxicity and Metabolic Stress in Cultured Hepatocytes.

OBJECTIVES: Metabolic overload caused by excessive fructose intake has been associated with hepatic disorders via oxidative stress and inflammation. Unregulated fructose metabolism leads to lipid accumulation and consequent reactive oxygen species (ROS) generation, thereby contributing to Nonalcoholic fatty liver disease (NAFLD). The present study aimed to investigate the potential of Coconut Haustorium (CH) against fructose-induced redox imbalance and lipotoxicity in HepG2 cells. METHODS: The cultured HepG2 cells were pretreated with biologically safer doses of CH prior to fructose (5 mM) exposure. Cellular antioxidant levels, inflammatory cytokines, lipid profile, and liver function parameters were assessed using commercial kits. RESULTS: Fructose exposure induced dyslipidemia, redox imbalance, and elevated levels of inflammatory cytokines, including TNF-α, IL-6, and IL-1β, in HepG2 cells. Corroborating these, the increased liver function marker enzyme activities highlight fructose-induced metabolic stress in hepatocytes. Treatment with coconut haustorium extract (10, 25, and high 50 𝜇g/mL) significantly attenuated fructose-induced oxidative damage and lipid accumulation. Treatment with CH (50 𝜇g/mL) restored the redox balance by improving antioxidant enzyme activities and by reducing TBARS levels (p < 0.001). In addition, a significant reduction (p < 0.001) in lipid content through elevation of HDLc levels was observed; these results were also evident in terms of improved liver function marker enzymes (p < 0.001) and reduced inflammation. HR-LC-MS/MS analysis confirmed the presence of compounds including phenolic acids, flavonoids, tannins, and triterpenoids, which might be responsible for the observed bioactivities of the CH. CONCLUSION: Overall, the results of the present study suggest that Coconut Haustorium possesses significant potential as a functional food ingredient capable of modulating intracellular redox homeostasis and lipotoxicity, thereby helping to prevent the progression of NAFLD.