Eicosapentaenoic acid enhances heat stress-impaired intestinal epithelial barrier function in Caco-2 cells.
Eicosapentaenoic acid enhances heat stress-impaired intestinal epithelial barrier function in Caco-2 cells.
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二十碳五烯酸增强 Caco-2 细胞中因热应激受损的肠上皮屏障功能
DOI：
10.1371/journal.pone.0073571
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Su L
中科院分区：
文献类型：
--
作者：
Xiao G;Tang L;Yuan F;Zhu W;Zhang S;Liu Z;Geng Y;Qiu X;Zhang Y;Su L
Objective Dysfunction of the intestinal epithelial tight junction (TJ) barrier is known to have an important etiologic role in the pathophysiology of heat stroke. N-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), play a role in maintaining and protecting the TJ structure and function. This study is aimed at investigating whether n-3 PUFAs could alleviate heat stress-induced dysfunction of intestinal tight junction. Methods Human intestinal epithelial Caco-2 cells were pre-incubated with EPA, DHA or arachidonic acid (AA) and then exposed to heat stress. Transepithelial electrical resistance (TEER) and Horseradish Peroxidase (HRP) permeability were measured to analyze barrier integrity. Levels of TJ proteins, including occludin, ZO-1 and claudin-2, were analyzed by Western blot and localized by immunofluorescence microscopy. Messenger RNA levels were determined by quantitative real time polymerase chain reaction (Q-PCR). TJ morphology was observed by transmission electron microscopy. Results EPA effectively attenuated the decrease in TEER and impairment of intestinal permeability in HRP flux induced by heat exposure. EPA significantly elevated the expression of occludin and ZO-1, while DHA was less effective and AA was not at all effective. The distortion and redistribution of TJ proteins, and disruption of morphology were also effectively prevented by pretreatment with EPA. Conclusion This study indicates for the first time that EPA is more potent than DHA in protecting against heat-induced permeability dysfunction and epithelial barrier damage of tight junction.
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影响因子：
6.3
作者：
Mickleborough, Timothy D.;Tecklenburg, Sandra L.;Lindley, Martin R.
通讯作者：
Lindley, Martin R.
影响因子：
6.3
作者：
Grau-Carmona, Teodoro;Moran-Garcia, Vicente;Acosta, Jose
通讯作者：
Acosta, Jose
影响因子：
3.3
作者：
Lambert, GP;Broussard, LJ;Gisolfi, CV
通讯作者：
Gisolfi, CV
影响因子：
--
作者：
Dörfel MJ;Huber O
通讯作者：
Huber O
影响因子：
9.3
作者：
Bischoff SC
通讯作者：
Bischoff SC