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热应激预处理通过p38信号通路减少脂多糖诱导的人脐静脉内皮细胞凋亡。

Heat stress pretreatment decreases lipopolysaccharide-induced apoptosis via the p38 signaling pathway in human umbilical vein endothelial cells.

作者信息

Liu Zhifeng, Zhong Tianyu, Zheng Dong, Cepinskas Inga, Peng Tianqing, Su Lei

机构信息

Department of Intensive Care Unit, General Hospital of Guangzhou Military Command, Guangzhou, Guangdong 510010, P.R. China.

Critical Illness Research Centre, Lawson Health Research Institute, University of Western Ontario, London, ON N6A 4G5, Canada.

出版信息

Mol Med Rep. 2016 Jul;14(1):1007-13. doi: 10.3892/mmr.2016.5303. Epub 2016 May 18.

Abstract

The present study aimed to investigate vascular endothelial apoptosis, and the regulatory molecules involved in the condition of heatstroke caused by direct hyperthermia due to high core temperature and gut‑derived endotoxemia. Human umbilical vascular endothelial cells (HUVECs) were isolated and treated with heat stress (43˚C for 1 h), lipopolysaccharide (LPS; 1 µg/ml), or a combination of heat stress pretreatment followed by LPS. Caspase‑3 activity, DNA fragmentation, and cell viability, determined using a 3‑(4, 5‑dimethyl thiazol‑2‑yl)‑2,5‑diphenyl tetrazolium bromide assay, were measured to examine cellular apoptosis. Changes in the expression levels of heat shock protein (HSP) 27, HSP90 and B‑cell lymphoma 2 (Bcl‑2), and the phosphorylation of p38 were detected using Western blot assays. The specific inhibitor of p38, SB203580, was also used. LPS induced endothelial apoptosis, as indicated by increased caspase‑3 activity, a high level of DNA fragmentation and low cell viability. LPS also increased p38 phosphorylation and decreased the expression levels of HSP27, HSP90 and Bcl‑2. Heat stress pretreatment inhibited LPS‑induced cellular apoptosis, increased the phosphorylation of p38, and increased the expression levels of HSP27, HSP90 and Bcl‑2. Pretreatment with SB203580 had effects similar to those of heat stress in the amelioration of LPS‑induced effects. These findings demonstrated that heat stress pretreatment decreased LPS‑induced Bcl‑2‑associated apoptosis in HUVECs by attenuating p38 activation, thereby increasing the expression levels of HSP27 and HSP90.

摘要

本研究旨在探讨血管内皮细胞凋亡以及在因核心体温过高导致的直接热疗和肠道源性内毒素血症引起的中暑情况下涉及的调节分子。分离人脐静脉血管内皮细胞(HUVECs),并分别用热应激(43˚C处理1小时)、脂多糖(LPS;1μg/ml)或热应激预处理后再给予LPS的组合进行处理。使用噻唑蓝比色法测定细胞凋亡相关指标,包括半胱天冬酶-3活性、DNA片段化和细胞活力。通过蛋白质免疫印迹法检测热休克蛋白(HSP)27、HSP90和B细胞淋巴瘤-2(Bcl-2)的表达水平变化以及p38的磷酸化情况。还使用了p38的特异性抑制剂SB203580。结果显示,LPS诱导内皮细胞凋亡,表现为半胱天冬酶-3活性增加、高水平的DNA片段化和低细胞活力。LPS还增加了p38磷酸化,并降低了HSP27、HSP90和Bcl-2的表达水平。热应激预处理可抑制LPS诱导的细胞凋亡,增加p38磷酸化,并增加HSP27、HSP90和Bcl-2的表达水平。用SB203580预处理产生的效果与热应激在改善LPS诱导效应方面的效果相似。这些研究结果表明,热应激预处理通过减弱p38激活,从而增加HSP27和HSP90的表达水平,减少了LPS诱导的HUVECs中与Bcl-2相关的细胞凋亡。

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