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多不饱和脂肪酸在幽门螺杆菌感染的胃上皮细胞中的抗炎机制。

Anti-inflammatory mechanism of polyunsaturated fatty acids in Helicobacter pylori-infected gastric epithelial cells.

作者信息

Lee Sun Eun, Lim Joo Weon, Kim Jung Mogg, Kim Hyeyoung

机构信息

Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 120-749, Republic of Korea.

Department of Microbiology, Hanyang University College of Medicine, Seoul 133-791, Republic of Korea.

出版信息

Mediators Inflamm. 2014;2014:128919. doi: 10.1155/2014/128919. Epub 2014 Jun 2.

DOI:10.1155/2014/128919
PMID:24987192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4060060/
Abstract

Helicobacter pylori is an important risk factor for gastric inflammation, which is mediated by multiple signaling pathways. The aim of this study was to investigate the effects of polyunsaturated fatty acids (PUFAs), such as linoleic acid (LA), alpha-linolenic acid (ALA), and docosahexaenoic acid (DHA), on the expression of the proinflammatory chemokine interleukin-8 (IL-8) in H. pylori-infected gastric epithelial AGS cells. To investigate whether PUFAs modulate H. pylori-induced inflammatory signaling, we determined the activation of epidermal growth factor receptor (EGFR), protein kinase C-δ (PKC δ), mitogen-activated protein kinases (MAPKs), nuclear factor-kappa B (NF- κB), and activator protein-1 (AP-1) as well as IL-8 expression in H. pylori-infected gastric epithelial cells that had been treated with or without PUFAs. We found that PUFAs inhibited IL-8 mRNA and protein expression in H. pylori-infected cells. ω-3 fatty acids (ALA, and DHA) suppressed the activation of EGFR, PKC δ, MAPK, NF- κB, and AP-1 in these infected cells. LA did not prevent EGFR transactivation and exhibited a less potent inhibitory effect on IL-8 expression than did ALA and DHA. In conclusion, PUFAs may be beneficial for prevention of H. pylori-associated gastric inflammation by inhibiting proinflammatory IL-8 expression.

摘要

幽门螺杆菌是胃炎症的一个重要风险因素,其由多种信号通路介导。本研究的目的是调查多不饱和脂肪酸(PUFAs),如亚油酸(LA)、α-亚麻酸(ALA)和二十二碳六烯酸(DHA),对幽门螺杆菌感染的胃上皮AGS细胞中促炎趋化因子白细胞介素-8(IL-8)表达的影响。为了研究PUFAs是否调节幽门螺杆菌诱导的炎症信号,我们测定了在已用或未用PUFAs处理的幽门螺杆菌感染的胃上皮细胞中表皮生长因子受体(EGFR)、蛋白激酶C-δ(PKC δ)、丝裂原活化蛋白激酶(MAPKs)、核因子-κB(NF-κB)和活化蛋白-1(AP-1)的激活情况以及IL-8的表达。我们发现PUFAs抑制了幽门螺杆菌感染细胞中IL-8的mRNA和蛋白表达。ω-3脂肪酸(ALA和DHA)抑制了这些感染细胞中EGFR、PKC δ、MAPK、NF-κB和AP-1的激活。LA不能阻止EGFR的反式激活,并且对IL-8表达的抑制作用比ALA和DHA弱。总之,PUFAs可能通过抑制促炎的IL-8表达而有利于预防幽门螺杆菌相关的胃炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/8132045b1ac0/MI2014-128919.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/487534a222c3/MI2014-128919.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/9a9241129db0/MI2014-128919.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/b004a48b57b7/MI2014-128919.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/01b48498b3b9/MI2014-128919.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/41e36c104a85/MI2014-128919.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/8132045b1ac0/MI2014-128919.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/487534a222c3/MI2014-128919.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/9a9241129db0/MI2014-128919.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/10e27a25d968/MI2014-128919.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/b004a48b57b7/MI2014-128919.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/41e36c104a85/MI2014-128919.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/733f/4060060/8132045b1ac0/MI2014-128919.007.jpg

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