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内质网应激扰乱了大黄鱼()肠道和分离的肠道细胞中的脂质稳态并增强了炎症反应。

Endoplasmic Reticulum Stress Disturbs Lipid Homeostasis and Augments Inflammation in the Intestine and Isolated Intestinal Cells of Large Yellow Croaker ().

机构信息

Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture and Rural Affairs) and Key Laboratory of Mariculture (Ministry of Education), Ocean University of China, Qingdao, China.

Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao, China.

出版信息

Front Immunol. 2021 Aug 19;12:738143. doi: 10.3389/fimmu.2021.738143. eCollection 2021.

Abstract

The small intestine is crucial for lipid homeostasis and immune regulation of the whole body. Endoplasmic reticulum (ER) stress may affect lipid metabolism and inflammation in the intestine, but the potential mechanism is not completely understood. In the present study, intraperitoneal injection of tunicamycin (TM) induced ER stress in the intestine of large yellow croaker (). ER stress induced excessive accumulation of triglyceride (TG) in the intestine by promoting lipid synthesis. However, it also enhanced lipid secretion and fatty acid β-oxidation. In addition, ER stress augmented inflammation in the intestine by promoting p65 into the nucleus and increasing proinflammatory genes expression. In the isolated intestinal cells, the obtained results showed that TM treatment significantly upregulated the mRNA expression of lipid synthesis and inflammatory response genes, which were consistent with those . Moreover, overexpression of unfolded protein response (UPR) sensors significantly upregulated promoter activities of lipid synthesis and proinflammatory genes. In conclusion, the results suggested that ER stress disturbed lipid metabolism and augmented inflammation in the intestine and isolated intestinal cells of large yellow croaker, which may contribute to finding novel therapies to tackle lipid dysregulation and inflammation in the intestine of fish and human beings.

摘要

小肠对于全身的脂质稳态和免疫调节至关重要。内质网(ER)应激可能会影响肠道中的脂质代谢和炎症,但潜在的机制尚不完全清楚。在本研究中,腹腔注射衣霉素(TM)诱导大黄鱼()肠道发生 ER 应激。ER 应激通过促进脂质合成,导致肠道中甘油三酯(TG)过度积累。然而,它也增强了脂质的分泌和脂肪酸β氧化。此外,ER 应激通过促进 p65 进入细胞核并增加促炎基因的表达,加剧了肠道炎症。在分离的肠细胞中,获得的结果表明,TM 处理显著上调了脂质合成和炎症反应基因的 mRNA 表达,与在整体肠组织中的结果一致。此外,UPR 传感器的过表达显著上调了脂质合成和促炎基因的启动子活性。总之,这些结果表明 ER 应激扰乱了大黄鱼肠道和分离的肠细胞中的脂质代谢并加剧了炎症,这可能有助于寻找新的治疗方法来解决鱼类和人类肠道中的脂质失调和炎症问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9873/8417523/165c2db31755/fimmu-12-738143-g001.jpg

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