Study On Mitochondrial Membrane Potential,Antioxidant Capacity And Apoptosis In Goose Fatty Liver

Landes geese can deposit large amounts of fat to form fatty liver after overfeeding,but there are no obvious pathological changes,suggesting that there may be a unique protective mechanism in goose fatty liver.The development of mammalian nonalcoholic fatty liver disease(NAFLD)is accompanied by oxidative stress,reduced mitochondrial function,and increased apoptosis of hepatocytes,yet the expression of mitochondria-related genes is elevated in goose fatty liver,suggesting that mitochondria may be involved in the tolerance mechanism of goose fatty liver.In view of this,this paper mainly focuses on the study of apoptosis-related gene expression and changes in mitochondrial membrane potential levels in goose fatty liver and the antioxidant capacity of goose fatty liver and its mitochondria from the perspective of goose liver cell mitochondria;the study of the effect of fatty liver formation-related factor glucose on apoptosis levels and antioxidant capacity of goose and mouse primary hepatocytes,and its effect on mitochondrial membrane potential and ROS levels in goose primary hepatocytes.The main findings were as follows:(1)Antioxidant capacity was increased in goose fatty liver,mitochondrial membrane potential was normal,and apoptotic gene expression was not changed.Overfeeding had no effect on the mRNA and protein expression levels of apoptosis-related genes Bcl-2,Bax and Caspase-3,and no effect on the mRNA level of Caspase-9 and protein level of cleaved Caspase-9 in the liver of goose,but it increased the mitochondrial membrane potential level very significantly(P<0.01).Filling of goose livers significantly reduced malondialdehyde(MDA)content(P<0.01)and significantly increased glutathione peroxidase(GSH-Px)activity and glutathione(GSH)content(P<0.01).This suggests that goose fatty liver may maintain normal mitochondrial membrane potential by increasing antioxidant capacity and thus resist the occurrence of apoptosis in goose liver cells.(2)No increase in the level of apoptosis occurred after glucose treatment of goose primary hepatocytes.Glucose treatment of primary hepatocytes revealed that 60 mM glucose significantly inhibited the mRNA expression levels of Bax and significantly induced the mRNA expression levels of Caspase-9 in goose primary hepatocytes(P<0.05),which had no significant effect on the mRNA and protein expression levels of Bcl-2,Bax and Caspase-3 in goose primary hepatocytes,and had no significant effect on the protein levels of cleaved Caspase-9 protein levels were also not significantly affected.However,apoptosis occurred in murine primary hepatocytes after glucose treatment.40 and 60 mM glucose significantly or significantly increased the mRNA expression levels of Bcl-2,Bax,Caspase-3 and Caspase-9 in murine primary hepatocytes(P<0.05).Glucose significantly reduced ROS levels in goose primary hepatocytes(P<0.01),but had no significant effect on mitochondrial membrane potential levels.40 mM glucose significantly increased the mRNA expression levels of GPX1 and GPX2(P<0.05)and SOD1(P<0.01)in goose primary hepatocytes;60 mM glucose significantly increased the mRNA expression levels of GPX1 and GPX2(P<0.05)and SOD1(P<0.01)in goose primary hepatocytes.60 mM glucose significantly increased the mRNA expression levels of GPX2(P<0.05),SOD1 and GPX1(P<0.01),and 20 mM glucose significantly increased the mRNA expression levels of GPX2(P<0.05)in goose primary hepatocytes,but none of the glucose treatments had significant effects on the mRNA expression levels of Nrf2.40 mM glucose significantly increased the mRNA expression levels of Nrf2.40 mM glucose significantly increased the mRNA expression level of GPX2(P<0.05)and significantly inhibited the mRNA expression level of Nrf2 gene(P<0.05)in mouse primary hepatocytes;60 mM glucose significantly increased the mRNA expression level of GPX1 and GPX2(P<0.01),but also significantly inhibited the mRNA expression level of Nrf2 gene(P<0.05).This indicates that mouse primary hepatocytes are intolerant to high glucose treatment and may have developed cellular damage.It indicates that goose primary hepatocytes are able to maintain normal mitochondrial function by increasing the expression of antioxidant genes to go against the onset of glucoseinduced apoptosis.In conclusion,no apoptosis was observed in both goose fatly liver and glucose-treated goose primary hepatocytes,and their antioxidant indexes were improved and mitochondrial function was normal.However,apoptosis occurred in murine primary hepatocytes after glucose treatment,and the expression of some antioxidant genes was inhibited.It is suggested that goose fatty liver may maintain normal mitochondrial function by increasing the antioxidant index,and then resist apoptosis caused by elevated glucose.