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通过激活 HepG2 细胞中的 LKB1/AMPK 途径抑制油酸诱导的脂质积累。

Suppresses Oleic Acid-Induced Lipid Accumulation through an Activation of LKB1/AMPK Pathway in HepG2 Cells.

作者信息

Kwon Eun-Bin, Kang Myung-Ji, Kim Soo-Yeon, Lee Yong-Moon, Lee Mi-Kyeong, Yuk Heung Joo, Ryu Hyung Won, Lee Su Ui, Oh Sei-Ryang, Moon Dong-Oh, Lee Hyun-Sun, Kim Mun-Ock

机构信息

Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Chungbuk 28116, Republic of Korea.

College of Pharmacy, Chungbuk National University, Cheongju, Chungbuk 28644, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2018 Jan 8;2018:3140267. doi: 10.1155/2018/3140267. eCollection 2018.

DOI:10.1155/2018/3140267
PMID:29507591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5817260/
Abstract

(ZA) has been used as folk medicines in East Asian and recently reported to have several bioactivity; however, the studies of ZA on the regulation of triacylglycerol (TG) biosynthesis have not been elucidated yet. In this study, we examined whether the methanol extract of ZA (ZA-M) could reduce oleic acid- (OA-) induced intracellular lipid accumulation and confirmed its mode of action in HepG2 cells. ZA-M was shown to promote the phosphorylation of AMPK and its upstream LKB1, followed by reduction of lipogenic gene expressions. As a result, treatment of ZA-M blocked de novo TG biosynthesis and subsequently mitigated intracellular neutral lipid accumulation in HepG2 cells. ZA-M also inhibited OA-induced production of reactive oxygen species (ROS) and TNF-, suggesting that ZA-M possess the anti-inflammatory feature in fatty acid over accumulated condition. Taken together, these results suggest that ZA-M attenuates OA-induced lipid accumulation and inflammation through the activation of LKB1/AMPK signaling pathway in HepG2 cells.

摘要

紫锥菊(ZA)在东亚地区一直被用作民间药物,最近有报道称其具有多种生物活性;然而,ZA对三酰甘油(TG)生物合成调控的研究尚未阐明。在本研究中,我们检测了紫锥菊甲醇提取物(ZA-M)是否能减少油酸(OA)诱导的细胞内脂质积累,并在HepG2细胞中证实了其作用模式。结果表明,ZA-M能促进AMPK及其上游LKB1的磷酸化,随后降低脂肪生成基因的表达。因此,ZA-M处理可阻断HepG2细胞中从头合成TG的过程,并随后减轻细胞内中性脂质的积累。ZA-M还抑制了OA诱导的活性氧(ROS)和肿瘤坏死因子-α(TNF-α)的产生,表明ZA-M在脂肪酸过度积累的情况下具有抗炎特性。综上所述,这些结果表明ZA-M通过激活HepG2细胞中的LKB1/AMPK信号通路减轻OA诱导的脂质积累和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/df2c70992392/ECAM2018-3140267.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/7ceba8689fd5/ECAM2018-3140267.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/12578a09336b/ECAM2018-3140267.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/ffeb6c21ba1e/ECAM2018-3140267.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/df0e497f801a/ECAM2018-3140267.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/ab0f252e491d/ECAM2018-3140267.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/df2c70992392/ECAM2018-3140267.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/7ceba8689fd5/ECAM2018-3140267.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/12578a09336b/ECAM2018-3140267.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/ffeb6c21ba1e/ECAM2018-3140267.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/df0e497f801a/ECAM2018-3140267.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/ab0f252e491d/ECAM2018-3140267.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad01/5817260/df2c70992392/ECAM2018-3140267.006.jpg

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