Leng Liang, Jiang Zhuo-Qin, Ji Gui-Yuan
Guangdong Provincial Key Laboratory of Nutrition and Health, Department of Nutrition, College of Public Health, Sun Yat-Sen University, Guangzhou 510080, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2011 Apr;45(4):335-9.
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.
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.
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).
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.
研究大豆异黄酮对非酒精性脂肪肝大鼠肝脏脂质、血脂、抗氧化指标及肝脏脂质代谢相关因子的影响。
将36只雄性SD大鼠按体重随机分为四组:正常对照组、非酒精性脂肪性肝病(NAFLD)模型对照组、低剂量异黄酮治疗组(10 mg/kg)和高剂量异黄酮组(20 mg/kg),每组9只。正常对照大鼠喂饲D12450B(脂肪能量为10%),模型对照和异黄酮干预大鼠喂饲D12492(脂肪能量为60%)。12周后,观察肝脏脂质、血脂及抗氧化指标。采用蛋白质免疫印迹法检测肝脏固醇调节元件结合蛋白-1c(SREBP-1c)、脂肪酸合酶(FAS)和过氧化物酶体增殖物激活受体α(PPARα)。
正常对照组、NAFLD模型对照组、低剂量异黄酮组和高剂量异黄酮组肝脏甘油三酯(TG)分别为(8.11±4.13)、(57.06±16.95)、(31.26±10.48)、(31.38±13.25)mmol/mg蛋白(F = 22.569,P < 0.01);肝脏游离脂肪酸(FFA)分别为(0.030±0.007)、(0.042±0.009)、(0.038±0.009)、(0.032±0.005)μmol/mg蛋白(F = 4.857,P < ;0.01);肝脏超氧化物歧化酶(SOD)活性分别为(502.29±23.71)、(201.83±16.99)、(228.93±21.71)、(238.08±15.96)U/mg蛋白(F = 9.555,P < 0.01);肝脏丙二醛(MDA)分别为(1.29±0.29)、(2.85±0.73)、(2.07±0.49)、(2.03±0.37)nmol/mg蛋白(F = 13.449,P < 0.01);SREBP-1c蛋白表达分别为0.45±0.16、1.42±0.30、1.02±0.31、0.47±0.27(F = 24.515,P < 0.01);FAS蛋白表达分别为0.27±0.08、1.97±0.47、1.35±0.30、0.49±0.12(F = 60.361,P < 0.01);PPARα蛋白表达分别为2.03±0.56、0.41±0.17、0.81±0.27、0.66±0.16(F = 37.97,P < 0.01)。
大豆异黄酮可减少肝脏脂质沉积并提高抗氧化能力,其机制可能与抑制肝脏SREBP-1c表达及激活PPARα表达有关。