大豆异黄酮对大鼠肝脏脂肪酸代谢的影响

Effects of Soy Isoflavone on Hepatic Fatty Acid Metabolism of Rats

【目的】研究不同剂量大豆异黄酮对大鼠肝脏脂肪酸代谢的影响并对其机理进行探讨。【方法】试验选取40只6周龄SD大鼠并随机分为对照组和低、中、高剂量组,每组10只。将不同剂量的大豆异黄酮(0、50、250、500 mg/kg)连续4周经口灌胃并记录大鼠每周体重变化;利用荧光定量PCR检测大鼠肝脏中固醇调节元件结合蛋白1(SREBP-1c)、乙酰辅酶A羧化酶α(ACC1)、脂肪酸合成酶(FAS)、过氧化物酶体增殖物激活受体α(PPARα)以及甘油三酯水解酶(ATGL)mRNA表达水平。【结果】与对照组相比,中、高剂量组大鼠体重极显著(P<0.01)降低并呈剂量依赖性;低剂量组甘油三酯含量显著下降(P<0.05),中剂量组总胆固醇、甘油三酯和低密度脂蛋白含量显著下降(P<0.05),高剂量组甘油三酯和低密度脂蛋白含量极显著下降(P<0.01);肝脏HE染色未见异常病理变化,油红O染色可见中、高剂量组脂滴明显减少;低剂量组大鼠肝脏中FAS、ACC1 mRNA表达量显著降低(P<0.01),中、高剂量组FAS、SREBP-1C和ACC-1mRNA表达量显著降低(P<0.05或P<0.01),而PPARα和ATGL mRNA表达量显著升高(P<0.05或P<0.01)。【结论】大豆异黄酮可通过抑制SREBP-1c、ACC1和FAS,增加ATGL和PPARα的基因表达,从而影响肝脏脂肪酸代谢。

【Objective】The experiment was designed to study the effects of different doses of soy isoflavoneson fatty acid metabolism of rat liver and its mechanism.【Method】Forty rats in 6 month were randomlydivided into control, low, middle and high groups,ten rats per group. The rats were given by gavagedifferent doses of soy isoflavones （0, 50, 250, 500 mg/kg） last for 4 weeks, and recorded the body weight everyweek; RT-PCR were used to test the mRNA levels of SREBP-1c,ACC1,FAS,PPAR and ATGL.【Result】The results showed that： compared with control group, rats in middle and high groups exhibiteddecreased body weight（P〈0.01）. TG in low group rats decreased significantly（P〈0.05）,TC,TG and LDL-cdecreased in middle group（P〈0.05）, TG and LDL-c extremely decreased in high group（P〈0.01）; No ab-normal pathological changes in liver by HE staining, but there were little lipid droplets left in the liver ofmiddle and high group rats by oil red staining; the mRNA expression of FAS, ACC1 in liver was significantlydecreased in low group rats（P〈0.01）,and FAS, SREBP-1C and ACC-1mRNA were also decreasedamong middle and high groups（P〈0.05 or P〈0.01）,however,the levels of PPAR and ATGL were signif-icantly increased（P〈0.05 or P〈0.01）.【Conclusion】All the results indicated that soy isoflavones can affecthepatic fatty acid metabolism by down-regulation the expression of SREBP-1c,ACC1 and FAS,butpromoting the expression of SREBP-1c,ACC1 and FAS.