Objective: To study the effects of soybean isoflavone on liver lipid, serum lipid, antioxidant index and hepatic lipid metabolism associated factors in nonalcoholic fatty liver rats.
Methods: Thirty-six male rats (SD) were randomly divided into four groups by weight: normal control group, nonalcoholic fatty liver disease (NAFLD) model control group, low-dose isoflavone treatment group (10 mg/kg) and high-dose isoflavone group (20 mg/kg), 9 rats in each group. Normal control rats were fed with D12450B (10% fat energy), model control and isoflavone intervention rats were fed with D12492 (60% fat energy). Twelve weeks later, liver lipid, serum lipid and antioxidant index were observed. Liver sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS) and peroxisome proliferators activated receptor alpha (PPAR alpha) were detected by western blotting.
Results: Liver triglyceride (TG) in normal control group, NAFLD model control group, low-dose isoflavone group and high-dose isoflavone group were (8.11 ± 4.13), (57.06 ± 16.95), (31.26 ± 10.48), (31.38 ± 13.25) mmol/mg protein, respectively (F = 22.569, P < 0.01); liver free fatty acid (FFA) were (0.030 ± 0.007), (0.042 ± 0.009), (0.038 ± 0.009), (0.032 ± 0.005) µmol/mg protein, respectively (F = 4.857, P < 0.01); liver superoxide dismutase (SOD) activity were (502.29 ± 23.71), (201.83 ± 16.99), (228.93 ± 21.71), (238.08 ± 15.96) U/mg protein, respectively (F = 9.555, P < 0.01); liver malondialdehyde (MDA) were (1.29 ± 0.29), (2.85 ± 0.73), (2.07 ± 0.49), (2.03 ± 0.37) nmol/mg protein, respectively (F = 13.449, P < 0.01); SREBP-1c protein expression were 0.45 ± 0.16, 1.42 ± 0.30, 1.02 ± 0.31, 0.47 ± 0.27, respectively (F = 24.515, P < 0.01); FAS protein expression were 0.27 ± 0.08, 1.97 ± 0.47, 1.35 ± 0.30, 0.49 ± 0.12, respectively (F = 60.361, P < 0.01); PPARα protein expression were 2.03 ± 0.56, 0.41 ± 0.17, 0.81 ± 0.27, 0.66 ± 0.16, respectively (F = 37.97, P < 0.01).
Conclusion: Soy isoflavone can reduce the hepatic lipid deposition and increase antioxidant capacity, the mechanism may be related to inhibition of SREBP-1c and activation of PPARα expression in liver.