In the present study, hepatoprotective effects were investigated in HepG2 cells over-expressing CYP2E1, with the pretreatment of flavonoids against ethanol; naringenin (NA), luteolin (LU), genistein (GE), kaempferol (KA), and quercetin (QU). The oxidative stress induced by ethanol caused a drastic...
In the present study, hepatoprotective effects were investigated in HepG2 cells over-expressing CYP2E1, with the pretreatment of flavonoids against ethanol; naringenin (NA), luteolin (LU), genistein (GE), kaempferol (KA), and quercetin (QU). The oxidative stress induced by ethanol caused a drastic decrease in cell viability with approximately 60%, while no cell death was observed when the HepG2-2E1 cells were pretreated with KA and QU (100% of cell viability). On the other hand, the treatment of other flavonoids did not prevent cell death from oxidative stress in comparison to the ethanol-alone treated group. Treatment of tested flavonoids (NA, LU, GE, KA, and QU) significantly reduced the intracellular ROS level compared to the ethanol-alone treated group, while only KA and QU decreased the TG level. The pretreatment with flavonoids (NA, LU, GE, KA, and QU) to the cells resulted in a significant increase in glutathione (GSH) level compared to the only ethanol?treated cells. Activities of the antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) were significantly decreased in only ethanol-alone treated cells compared to normal control group. On the basis of the results, the mice administered with KA and QU (50 mg/kg b.w./day) plus ethanol for 3 days had significantly reduced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activities compared to ethanol-alone administered mice (5 g/kg b.w./day of ethanol), as well as serum triglyceride (TG). The oral administration with KA and QU to the mice resulted in the significant improvement on the weakened antioxdative defense system in mice challenged with ethanol. These results suggest that flavonoids attenuate oxidative stress by improving antioxidative potentials. In vitro and in vivo studies with KA and QU showed the relatively high hepatoprotective effect compared to the ethanol group, as indicated by the restoration of CYP2E1, PPAR-α, SREBP-1, AMPK, ACC, and CPT-1 expressions. Based upon these results, KA and QU might possess the protective effect against the liver damage mediated by ethanol via the alleviation of oxidative stress and the prevention of steatosis.
In the present study, hepatoprotective effects were investigated in HepG2 cells over-expressing CYP2E1, with the pretreatment of flavonoids against ethanol; naringenin (NA), luteolin (LU), genistein (GE), kaempferol (KA), and quercetin (QU). The oxidative stress induced by ethanol caused a drastic decrease in cell viability with approximately 60%, while no cell death was observed when the HepG2-2E1 cells were pretreated with KA and QU (100% of cell viability). On the other hand, the treatment of other flavonoids did not prevent cell death from oxidative stress in comparison to the ethanol-alone treated group. Treatment of tested flavonoids (NA, LU, GE, KA, and QU) significantly reduced the intracellular ROS level compared to the ethanol-alone treated group, while only KA and QU decreased the TG level. The pretreatment with flavonoids (NA, LU, GE, KA, and QU) to the cells resulted in a significant increase in glutathione (GSH) level compared to the only ethanol?treated cells. Activities of the antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) were significantly decreased in only ethanol-alone treated cells compared to normal control group. On the basis of the results, the mice administered with KA and QU (50 mg/kg b.w./day) plus ethanol for 3 days had significantly reduced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activities compared to ethanol-alone administered mice (5 g/kg b.w./day of ethanol), as well as serum triglyceride (TG). The oral administration with KA and QU to the mice resulted in the significant improvement on the weakened antioxdative defense system in mice challenged with ethanol. These results suggest that flavonoids attenuate oxidative stress by improving antioxidative potentials. In vitro and in vivo studies with KA and QU showed the relatively high hepatoprotective effect compared to the ethanol group, as indicated by the restoration of CYP2E1, PPAR-α, SREBP-1, AMPK, ACC, and CPT-1 expressions. Based upon these results, KA and QU might possess the protective effect against the liver damage mediated by ethanol via the alleviation of oxidative stress and the prevention of steatosis.
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