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黑果枸杞可减轻小鼠非酒精性脂肪肝。

Lycium ruthenicum Murr. alleviates nonalcoholic fatty liver in mice.

作者信息

Lu Keke, Wang Jing, Yu Yueyuan, Wu Yikuan, He Zhao

机构信息

Shandong Provincial Hospital and School of Medicine Shandong University Jinan China.

State Key Laboratory of Food Science and Technology School of Food Science and Technology Jiangnan University Wuxi China.

出版信息

Food Sci Nutr. 2020 Mar 18;8(6):2588-2597. doi: 10.1002/fsn3.1445. eCollection 2020 Jun.

DOI:10.1002/fsn3.1445
PMID:32566176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7300084/
Abstract

Oxidative stress and inflammation contribute to hypertriglyceridemia-induced nonalcoholic fatty liver disease (NAFLD). Cholesterol-enriched diets increase the risk of NAFLD. Murr. (LRM) contains water-soluble antioxidant proanthocyanidins. Whether Murr. improves NAFLD remains elusive. In this study, we established a model of NAFLD-induced by cholesterol-enriched high-fat diet (western diet) in mice; oxidative stress and inflammation were examined and intervened by supplement of Murr. (LRM) extracts. LRM supplement did not influence body weight gain, food intake, and lipotoxicity of mice. LRM supplement significantly alleviated triglyceride accumulation in liver, with reduced inflammation, elevated GSH-Px activity, and reduced MDA levels. The expression of fatty acids oxidative gene was significantly increased, and fatty acids synthesis-related gene was dramatically downregulated on mRNA level in liver of mice with LRM supplement. These data demonstrated that LRM supplement decreased ROS production and inflammation, increased fatty acids oxidation, and reduced fatty acids synthesis in liver, leading to ameliorate the development of NAFLD induced by high western diet. Thus, oxidative stress and inflammation also are involved in the pathogenesis of western diet-induced NAFLD, which is independent of obesity.

摘要

氧化应激和炎症促成了高甘油三酯血症诱导的非酒精性脂肪性肝病(NAFLD)。富含胆固醇的饮食会增加患NAFLD的风险。毛脉酸模(LRM)含有水溶性抗氧化剂原花青素。LRM是否能改善NAFLD仍不清楚。在本研究中,我们在小鼠中建立了由富含胆固醇的高脂肪饮食(西方饮食)诱导的NAFLD模型;通过补充毛脉酸模(LRM)提取物来检测和干预氧化应激和炎症。补充LRM不影响小鼠的体重增加、食物摄入量和脂毒性。补充LRM显著减轻了肝脏中的甘油三酯积累,炎症减轻,谷胱甘肽过氧化物酶(GSH-Px)活性升高,丙二醛(MDA)水平降低。在补充LRM的小鼠肝脏中,脂肪酸氧化基因的表达在mRNA水平上显著增加,而脂肪酸合成相关基因则显著下调。这些数据表明,补充LRM可减少肝脏中的活性氧(ROS)产生和炎症,增加脂肪酸氧化,并减少脂肪酸合成,从而改善由西方高糖饮食诱导的NAFLD的发展。因此,氧化应激和炎症也参与了西方饮食诱导的NAFLD的发病机制,这与肥胖无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/6c3ba6237962/FSN3-8-2588-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/0c5102b5d7e2/FSN3-8-2588-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/86b14b62a21a/FSN3-8-2588-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/3639d691e075/FSN3-8-2588-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/9019d814f497/FSN3-8-2588-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/6c3ba6237962/FSN3-8-2588-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/0c5102b5d7e2/FSN3-8-2588-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/86b14b62a21a/FSN3-8-2588-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/3639d691e075/FSN3-8-2588-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/9019d814f497/FSN3-8-2588-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b46/7300084/6c3ba6237962/FSN3-8-2588-g005.jpg

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