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α-山竹黄酮通过抑制C-C趋化因子受体2改善肝脂肪变性和胰岛素抵抗。

α-Mangostin ameliorates hepatic steatosis and insulin resistance by inhibition C-C chemokine receptor 2.

作者信息

Kim Hong Min, Kim You Mi, Huh Ji Hye, Lee Eun Soo, Kwon Mi Hye, Lee Bo Ra, Ko Hyun-Jeong, Chung Choon Hee

机构信息

Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.

Laboratory of Microbiology and Immunology, College of Pharmacy, Kangwon National University, Chuncheon, Korea.

出版信息

PLoS One. 2017 Jun 9;12(6):e0179204. doi: 10.1371/journal.pone.0179204. eCollection 2017.

DOI:10.1371/journal.pone.0179204
PMID:28598982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5466328/
Abstract

Obesity induces various metabolic diseases such as dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes. Fat expansion in adipose tissue induces adipose tissue dysfunction and inflammation, insulin resistance, and other metabolic syndromes. α-Mangostin (α-MG) has been previously studied for its anti-cancer, anti-inflammatory, and antioxidant activities. In this study, we investigated the effects of α-MG on adipose tissue inflammation and hepatic steatosis. We categorized study animals into four groups: regular diet control mice, RD mice treated with α-MG, high fat diet-induced obese mice, and HFD mice treated with α-MG. α-MG treatment significantly reduced not only the body, liver, and fat weights, but also plasma glucose, insulin, and triglyceride levels in HFD mice. Additionally, adiponectin levels of α-MG-treated mice were significantly higher than those of control HFD mice. Immunohistochemistry of liver and adipose tissue showed that CD11c expression was reduced in α-MG fed obese mice. α-MG treatment of HFD mice down-regulated the adipose-associated inflammatory cytokines and CCR2 in both liver and adipose tissue. Moreover, glucose tolerance and insulin sensitivity were significantly improved in α-MG fed obese mice. α-Mangostin ameliorates adipose inflammation and hepatic steatosis in HFD-induced obese mice.

摘要

肥胖会引发各种代谢性疾病,如血脂异常、非酒精性脂肪性肝病(NAFLD)和2型糖尿病。脂肪组织中的脂肪扩张会导致脂肪组织功能障碍和炎症、胰岛素抵抗以及其他代谢综合征。此前已对α-山竹素(α-MG)的抗癌、抗炎和抗氧化活性进行过研究。在本研究中,我们调查了α-MG对脂肪组织炎症和肝脂肪变性的影响。我们将实验动物分为四组:常规饮食对照小鼠、接受α-MG治疗的常规饮食小鼠、高脂饮食诱导的肥胖小鼠以及接受α-MG治疗的高脂饮食小鼠。α-MG治疗不仅显著降低了高脂饮食小鼠的体重、肝脏重量和脂肪重量,还降低了其血浆葡萄糖、胰岛素和甘油三酯水平。此外,接受α-MG治疗的小鼠脂联素水平显著高于高脂饮食对照小鼠。肝脏和脂肪组织的免疫组织化学显示,喂食α-MG的肥胖小鼠中CD11c表达降低。α-MG对高脂饮食小鼠的治疗下调了肝脏和脂肪组织中与脂肪相关的炎症细胞因子和CCR2。此外,喂食α-MG的肥胖小鼠的葡萄糖耐量和胰岛素敏感性显著改善。α-山竹素可改善高脂饮食诱导的肥胖小鼠的脂肪炎症和肝脂肪变性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/a21c999af124/pone.0179204.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/7fa27fba21c3/pone.0179204.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/fb54c65d96cd/pone.0179204.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/651ae1e8076f/pone.0179204.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/ef18e7a7e65f/pone.0179204.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/8d0144cc2696/pone.0179204.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/a8870cdbbcf3/pone.0179204.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/a21c999af124/pone.0179204.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/7fa27fba21c3/pone.0179204.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/fb54c65d96cd/pone.0179204.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/651ae1e8076f/pone.0179204.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/ef18e7a7e65f/pone.0179204.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/8d0144cc2696/pone.0179204.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/a8870cdbbcf3/pone.0179204.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcc/5466328/a21c999af124/pone.0179204.g007.jpg

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