Xu Jiqu, Rong Shuang, Gao Hui, Chen Chang, Yang Wei, Deng Qianchun, Huang Qingde, Xiao Lingyun, Huang Fenghong
Department of Nutriology, Oil Crops Research Institute, Chinese Academy of Agricultural Sciences, 2 Xudong Second Road, Wuhan 430062, China.
Hubei Key Laboratory of Lipid Chemistry and Nutrition, Oil Crops Research Institute, Chinese Academy of Agricultural Sciences, 2 Xudong Second Road, Wuhan 430062, China.
Nutrients. 2017 Mar 13;9(3):271. doi: 10.3390/nu9030271.
Hepatic lipid accumulation and oxidative stress are crucial pathophysiological mechanisms for non-alcoholic fatty liver disease (NAFLD). Thus, we examined the effect of a combination of flaxseed oil (FO) and astaxanthin (ASX) on hepatic lipid accumulation and oxidative stress in rats fed a high-fat diet. ASX was dissolved in flaxseed oil (1 g/kg; FO + ASX). Animals were fed diets containing 20% fat, where the source was lard, or 75% lard and 25% FO + ASX, or 50% lard and 50% FO + ASX, or FO + ASX, for 10 weeks. Substitution of lard with FO + ASX reduced steatosis and reduced hepatic triacylglycerol and cholesterol. The combination of FO and ASX significantly decreased hepatic sterol regulatory element-binding transcription factor 1 and 3-hydroxy-3-methylglutaryl-CoA reductase but increased peroxisome proliferator activated receptor expression. FO + ASX significantly suppressed fatty acid synthase and acetyl CoA carboxylase but induced carnitine palmitoyl transferase-1 and acyl CoA oxidase expression. FO + ASX also significantly elevated hepatic SOD, CAT and GPx activity and GSH, and markedly reduced hepatic lipid peroxidation. Thus, FO and ASX may reduce NAFLD by reversing hepatic steatosis and reducing lipid accumulation and oxidative stress.
肝脏脂质蓄积和氧化应激是非酒精性脂肪性肝病（NAFLD）的关键病理生理机制。因此，我们研究了亚麻籽油（FO）和虾青素（ASX）联合使用对高脂饮食喂养大鼠肝脏脂质蓄积和氧化应激的影响。将ASX溶解于亚麻籽油中（1 g/kg；FO + ASX）。动物分别喂食含20%脂肪（脂肪来源为猪油）、75%猪油和25% FO + ASX、50%猪油和50% FO + ASX或FO + ASX的饲料，持续10周。用FO + ASX替代猪油可减轻脂肪变性，并降低肝脏三酰甘油和胆固醇水平。FO和ASX联合使用可显著降低肝脏固醇调节元件结合转录因子1和3-羟基-3-甲基戊二酰辅酶A还原酶水平，但增加过氧化物酶体增殖物激活受体的表达。FO + ASX可显著抑制脂肪酸合酶和乙酰辅酶A羧化酶，但诱导肉碱棕榈酰转移酶-1和酰基辅酶A氧化酶的表达。FO + ASX还可显著提高肝脏超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性以及谷胱甘肽水平，并显著降低肝脏脂质过氧化。因此，FO和ASX可能通过逆转肝脏脂肪变性、减少脂质蓄积和氧化应激来减轻NAFLD。
