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宫内营养不良降低脂多糖刺激的雄性大鼠肺血管内皮细胞中长型瘦素受体异构体的表达和促炎细胞因子的产生。

Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide.

机构信息

Department of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, Brazil.

Biotério Central, Universidade de São Paulo, São Paulo, SP, Brazil.

出版信息

Mediators Inflamm. 2018 Jul 9;2018:8597361. doi: 10.1155/2018/8597361. eCollection 2018.

DOI:10.1155/2018/8597361
PMID:30116155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6079436/
Abstract

BACKGROUND/AIMS: We have previously shown that low birth weight (LBW) rats exposed to intrauterine malnutrition have an impaired lung inflammatory response and reduced levels of inflammatory mediators; however, circulating leptin levels were not increased. We evaluated long leptin receptor isoform (ObRb) expression in lung endothelial cells from low birth weight rats and examined its role in the production of lipid mediators and cytokines.

METHODS

Lung endothelial cells were obtained from normal birth weight (NBW) rats or LBW rats subjected to intrauterine malnutrition. These cells were stimulated with leptin (10 ng/mL), LPS (lipopolysaccharide, 1 g/mL), or leptin plus LPS. Six hours after stimulation, the production of inflammatory mediators (PGE, LTB, IL-1, and IL-6) was evaluated using commercial ELISA kits, and Western blotting was performed to investigate p38MAPK, NF-B, and ObRb expression.

RESULTS

Leptin increased IL-1 levels in only cells from the NBW group, whereas LPS increased PGE and LTB levels in cells from both groups; leptin addition potentiated lipid mediator production induced by LPS in the NBW group. LPS enhanced the production of IL-1 and IL-6 in only endothelial cells from NBW rats. Leptin receptor expression was decreased (63%) in endothelial cells from LBW rats. None of the stimuli increased NF-B or p38 signaling pathway expression in cells from LBW rats.

CONCLUSION

These results suggest that intrauterine malnutrition compromises leptin receptor expression and cytokine production in pulmonary endothelial cells stimulated by LPS; these effects seem to involve the NF-B and p38MAPK signaling pathways.

摘要

背景/目的：我们之前已经表明，宫内营养不良导致的低出生体重（LBW）大鼠的肺部炎症反应受损，炎症介质水平降低；然而，循环瘦素水平并未升高。我们评估了低出生体重大鼠肺内皮细胞中长瘦素受体异构体（ObRb）的表达，并研究了其在脂质介质和细胞因子产生中的作用。

方法

从正常出生体重（NBW）大鼠或宫内营养不良的 LBW 大鼠中获得肺内皮细胞。用瘦素（10ng/mL）、脂多糖（LPS，1μg/mL）或瘦素加 LPS 刺激这些细胞。刺激 6 小时后，使用商业 ELISA 试剂盒评估炎症介质（PGE、LTB、IL-1 和 IL-6）的产生，并通过 Western blot 法研究 p38MAPK、NF-B 和 ObRb 的表达。

结果

瘦素仅增加了 NBW 组细胞中 IL-1 的水平，而 LPS 增加了两组细胞中 PGE 和 LTB 的水平；瘦素的加入增强了 LPS 在 NBW 组中诱导的脂质介质的产生。LPS 仅增强了仅来自 NBW 大鼠内皮细胞的 IL-1 和 IL-6 的产生。LBW 大鼠内皮细胞中的瘦素受体表达降低了（63%）。LPS 未增加 LBW 大鼠细胞中 NF-B 或 p38 信号通路的表达。

结论

这些结果表明，宫内营养不良会损害 LPS 刺激的肺内皮细胞中瘦素受体的表达和细胞因子的产生；这些作用似乎涉及 NF-B 和 p38MAPK 信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/8d388fbe1260/MI2018-8597361.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/728ed96eb222/MI2018-8597361.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/36c6811bb5fa/MI2018-8597361.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/55fe25e4ee83/MI2018-8597361.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/20e82bd116fb/MI2018-8597361.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/2031473fd051/MI2018-8597361.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/ef62fc766681/MI2018-8597361.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/8d388fbe1260/MI2018-8597361.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/728ed96eb222/MI2018-8597361.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/36c6811bb5fa/MI2018-8597361.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/55fe25e4ee83/MI2018-8597361.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/20e82bd116fb/MI2018-8597361.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/2031473fd051/MI2018-8597361.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/ef62fc766681/MI2018-8597361.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/056b/6079436/8d388fbe1260/MI2018-8597361.007.jpg

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