| Objective: Nonalcoholic fatty liver disease(NAFLD)can be caused by many factors such as liver oxidative stress(OS),fat accumulation,lipotoxicity and mitochondrial dysfunction.Peroxisome proliferator-activated receptor γ coactivator-1(PGC-1α)is involved in the regulation of lipid metabolism.The transcription factors in the downstream such as nuclear respiration factor 1(NRF-1)and mitochondrial transcription factor(TFAM)are closely related to mitochondrial oxidative metabolism.The purpose of this study was to investigate whether LBP could modulate PGC-1α,NRF-1 and TFAM to protect non-alcoholic cells induced hepatic steatosis,and to observe its effects on alanine aminotransferase(ALT)and aspartate aminotransferase(AST)and adenosine triphosphate(ATP).Methods: After incubating LO2 cells(human normal liver cells)in vitro for 24 hours,the cells were divided into two groups: normal control group and modeling group;free fatty acids(oleic acid: palm acid = 2:1)were used in the modeling group induced hepatic steatosis,and successful model cells were divided into four groups: NAFLD model group(without LBP),LBP low intervention group(NAFLD cells + 30μg/mL LBP),and LBP medium intervention group(NAFLD cells + 100μg/m L LBP)and LBP high intervention group(NAFLD cells + 300μg/mL LBP),the number of lipid droplets in the cells was observed under light microscope and the ALT,AST was measured by microplate method.Ultraviolet Spectrophotometer determinate the mitochondrial function index ATP.The expression ofPGC-1α,NRF-1 and TFAM mRNA was detected by Real-time PCR and protein expression was detected by Western Blot.Results:Compared with the NAFLD model group,the number of lipid droplets in the normal control group and the LBP low,medium and high intervention group was less than the NAFLD model;The levels of ALT and AST in normal control group,LBP low intervention group,LBP middle intervention group and LBP high intervention were lower than those in the NAFLD model group(P<0.01);And the normal control group was higher than the LBP medium intervention group and the LBP high intervention group(P<0.01).Compared with the LBP high intervention group,the levels of ALT and AST were increased in the LBP low intervention group;compared with the NAFLD model group,the ATP level in the normal control group,LBP low intervention group of,LBP middle intervention group and the LBP high intervention group was increased(P<0.01);And ATP level in normal control group were lower than LBP medium intervention group and LBP high intervention group(P<0.01).ATP level in LBP low intervention group were lower than in LBP high intervention group;Compared with the NAFLD model group,the expression of PGC-1α,NRF-1 and TFAM gene and protein was increased in the normal control group,LBP low intervention group,LBP medium intervention group and LBP high intervention group(P<0.05);And the expression levels of PGC-1α,NRF-1 and TFAM in LBP medium intervention group and LBP high intervention group were higher than normal control group(P<0.01).Compared with each other,the expression of PGC-1α,NRF-1 and TFAM in the LBP high intervention group was higher than them in the LBP low intervention group(P<0.01).Conclusion: LBP can reduce lipid deposition in NAFLD cells,and up-regulate the expression of PGC-1α in NAFLD cells,and then up-regulate the expression of downstream factors NRF-1 and TFAM of PGC-1α,improve mitochondrial function and repair liver cell damage,also can reduce abnormal liver function indicators,plays a protective effection on liver cells. |