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光萼党参富含咖啡酰奎宁酸的提取物通过调节载脂蛋白E基因敲除小鼠的过氧化物酶体增殖物激活受体和脂联素改善非酒精性脂肪肝

Caffeoylquinic Acid-Rich Extract of F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPAR and Adiponectin in ApoE KO Mice.

作者信息

Lee Yong-Jik, Jang Yoo-Na, Han Yoon-Mi, Kim Hyun-Min, Jeong Jong-Min, Son Min Jeoung, Jin Chang Bae, Kim Hyoung Ja, Seo Hong Seog

机构信息

Cardiovascular Center, Korea University, Guro Hospital, 148 Gurodong-ro, Guro-gu, Seoul 08308, Republic of Korea.

Department of Medical Science, Korea University College of Medicine (BK21 Plus KUMS Graduate Program), Main Building 6F Room 655, 73 Inchon-ro (Anam-dong 5-ga), Seongbuk-gu, Seoul 136-705, Republic of Korea.

出版信息

PPAR Res. 2017;2017:3912567. doi: 10.1155/2017/3912567. Epub 2017 Oct 23.

DOI:10.1155/2017/3912567
PMID:29201040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5672637/
Abstract

is well known for its therapeutic properties. This study was performed to investigate the effects of on nonalcoholic fatty liver disease (NAFLD) in atherosclerotic condition, by determining the levels of biomarkers related to lipid metabolism and inflammation in serum, liver, and adipose tissue. Body and abdominal adipose tissue weights and serum triglyceride level decreased in all groups treated with . Serum adiponectin concentration and protein levels of peroxisome proliferator-activated receptor , 5' adenosine monophosphate-activated protein kinase, acetyl-CoA carboxylase, superoxide dismutase, and PPAR coactivator 1-alpha in liver tissues increased in the groups treated with . Conversely, protein levels of ATP citrate lyase, fatty acid synthase, tumor necrosis factor , and 3-hydroxy-3-methylglutaryl-CoA reductase and the concentrations of interleukin 6 and reactive oxygen species decreased upon . Triglyceride concentration in the liver was lower in mice treated with than in control mice. Lipid accumulation in HepG2 and 3T3-L1 cells decreased upon treatment; this effect was suppressed in the presence of the PPAR antagonist, GSK0660. Our findings suggest that extracts may ameliorate NAFLD through regulation of PPAR, adiponectin, and the related subgenes.

摘要

以其治疗特性而闻名。本研究旨在通过测定血清、肝脏和脂肪组织中与脂质代谢和炎症相关的生物标志物水平,研究其对动脉粥样硬化状态下非酒精性脂肪性肝病(NAFLD)的影响。所有接受治疗的组中,体重、腹部脂肪组织重量和血清甘油三酯水平均下降。接受治疗的组中,血清脂联素浓度以及肝脏组织中过氧化物酶体增殖物激活受体、5' 腺苷单磷酸激活蛋白激酶、乙酰辅酶A羧化酶、超氧化物歧化酶和PPAR共激活因子1-α的蛋白水平均升高。相反,经治疗后,ATP柠檬酸裂解酶、脂肪酸合酶、肿瘤坏死因子和3-羟基-3-甲基戊二酰辅酶A还原酶的蛋白水平以及白细胞介素6和活性氧的浓度均下降。接受治疗的小鼠肝脏中的甘油三酯浓度低于对照小鼠。经治疗后,HepG2和3T3-L1细胞中的脂质积累减少;在PPAR拮抗剂GSK0660存在的情况下,这种作用受到抑制。我们的研究结果表明,提取物可能通过调节PPAR、脂联素及相关亚基因来改善NAFLD。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/c1221f6c3ffa/PPAR2017-3912567.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/777e188c4172/PPAR2017-3912567.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/bc6160d8f58d/PPAR2017-3912567.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/26c721ad39b7/PPAR2017-3912567.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/c1221f6c3ffa/PPAR2017-3912567.010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/777e188c4172/PPAR2017-3912567.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/86f9b4754930/PPAR2017-3912567.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/5936cc54316b/PPAR2017-3912567.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/17964ea0b65e/PPAR2017-3912567.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/49092005b29a/PPAR2017-3912567.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/bc6160d8f58d/PPAR2017-3912567.008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405d/5672637/c1221f6c3ffa/PPAR2017-3912567.010.jpg

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