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水飞蓟籽油可减轻高脂饮食喂养小鼠的肝脂肪变性和氧化应激。

Silybum marianum oil attenuates hepatic steatosis and oxidative stress in high fat diet-fed mice.

机构信息

School of Food and Biological Engineering, Jiangsu University, Zhenjiang 212013, China; Jiangsu Hengshun Group Co., Ltd., Zhenjiang 212000, China.

Institute of Vegetables, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China.

出版信息

Biomed Pharmacother. 2018 Apr;100:191-197. doi: 10.1016/j.biopha.2018.01.144. Epub 2018 Feb 8.

DOI:10.1016/j.biopha.2018.01.144
PMID:29428667
Abstract

In the present study, the effects of Silybum marianum oil (SMO) on hepatic steatosis and oxidative stress were investigated during the development of nonalcoholic fatty liver disease (NAFLD) in high fat diet (HFD)-fed mice. The results showed that body weight, fat mass, and serum biochemical parameters such as triglyceride, free fatty acid, glucose and insulin were reduced by SMO treatment. Meanwhile, SMO decreased the histological injury of liver and the levels of hepatic triglyceride, cholesterol and free fatty acid in HFD-fed mice. SMO administration elevated the activities of superoxide dismutase (SOD) and catalase (CAT) and reduced the level of malondialdehyde (MDA) in the liver. Enzyme linked immunosorbent assay showed that SMO significantly decreased the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in HFD mice. Furthermore, the mRNA levels of sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and liver X receptor α (LXRα) were lower, but peroxisome proliferator-activated receptor α (PPARα) was higher in mice treated with SMO compared with the HFD group. The results indicated that SMO could play a certain protective role against HFD-induced NAFLD, and the protective effects might be associated with attenuating lipid accumulation, oxidative stress and inflammation, improving lipid metabolism.

摘要

在本研究中,研究了水飞蓟籽油(SMO)在高脂肪饮食(HFD)喂养的小鼠非酒精性脂肪性肝病(NAFLD)发展过程中对肝脂肪变性和氧化应激的影响。结果表明,SMO 处理可降低体重、脂肪量和血清生化参数(如甘油三酯、游离脂肪酸、葡萄糖和胰岛素)。同时,SMO 降低了 HFD 喂养小鼠的肝组织损伤和肝甘油三酯、胆固醇和游离脂肪酸水平。SMO 给药可提高超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性,并降低肝丙二醛(MDA)水平。酶联免疫吸附试验表明,SMO 可显著降低 HFD 小鼠肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的水平。此外,与 HFD 组相比,SMO 处理的小鼠固醇调节元件结合蛋白 1c(SREBP-1c)、脂肪酸合成酶(FAS)和肝 X 受体α(LXRα)的 mRNA 水平降低,而过氧化物酶体增殖物激活受体α(PPARα)水平升高。结果表明,SMO 可对 HFD 诱导的 NAFLD 发挥一定的保护作用,其保护作用可能与减轻脂质积累、氧化应激和炎症、改善脂质代谢有关。

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