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增强的白细胞介素-10通过脓毒症中的信号转导和转录激活因子3信号通路抑制人脐静脉内皮细胞的增殖并促进其凋亡。

Enhanced IL-10 inhibits proliferation and promotes apoptosis of HUVECs through STAT3 signaling pathway in sepsis.

作者信息

Xie Zuohua, Lin Bing, Jia Xinju, Su Ting, Wei Ying, Tang Jiping, Yang Chengzhi, Cui Chuanbao, Liu Jinxiang

机构信息

Department of Critical Care Medicine, The Third Affiliated Hospital of Guangxi Medical University, Nanning, PR China.

Graduate School, Guangxi Medical University, Nanning, PR China.

出版信息

Histol Histopathol. 2021 Nov;36(11):1179-1187. doi: 10.14670/HH-18-375. Epub 2021 Sep 16.

Abstract

AIMS

The present study aims to determine the expression of interleukin (IL)-10 in peripheral blood of patients with sepsis, and investigate its effects on the biological function of vascular endothelial cells.

METHODS

Thirty-six sepsis patients and 20 healthy subjects were included. Peripheral blood was collected from all subjects. ELISA was used to determine IL-10 content in serum. A ratio of IL-10⁺ T cells was determined by flow cytometry. CCK-8 assay was used to investigate proliferation. Cell cycle and apoptosis were analyzed by flow cytometry. Western blotting was used to examine the expression of phosphorylated STAT3 protein.

RESULTS

The content of IL-10 and the ratio of IL-10⁺ T cells were enhanced in pa-tients with sepsis. Serum from patients with sepsis inhibited the proliferation of HU-VECs, and addition of IL-10 antibody reversed this effect. IL-10 in the serum from patients with sepsis promoted the apoptosis of HUVECs. IL-10 inhibited the proliferation and promoted the apoptosis of HUVECs by enhancing the phosphorylation of STAT3.

CONCLUSIONS

The present study demonstrates that the content of IL-10 and the ratio of IL-10⁺ T cells in peripheral blood of patients with sepsis are up-regulated, and this inhibits HUVEC proliferation and promotes HUVEC apoptosis through STAT3 sig-naling pathway. The results in this study provide a new experimental basis for further understanding the molecular mechanism of sepsis-induced vascular injury.

摘要

目的

本研究旨在测定脓毒症患者外周血中白细胞介素(IL)-10的表达,并探讨其对血管内皮细胞生物学功能的影响。

方法

纳入36例脓毒症患者和20名健康受试者。采集所有受试者的外周血。采用酶联免疫吸附测定法(ELISA)测定血清中IL-10含量。通过流式细胞术测定IL-10⁺T细胞比例。采用细胞计数试剂盒-8(CCK-8)法检测细胞增殖情况。通过流式细胞术分析细胞周期和细胞凋亡。采用蛋白质免疫印迹法检测磷酸化信号转导和转录激活因子3(STAT3)蛋白的表达。

结果

脓毒症患者IL-10含量及IL-10⁺T细胞比例升高。脓毒症患者血清抑制人脐静脉内皮细胞(HUVECs)增殖,加入IL-10抗体可逆转此效应。脓毒症患者血清中的IL-10促进HUVECs凋亡。IL-10通过增强STAT3磷酸化抑制HUVECs增殖并促进其凋亡。

结论

本研究表明,脓毒症患者外周血中IL-10含量及IL-10⁺T细胞比例上调,且通过STAT3信号通路抑制HUVECs增殖并促进其凋亡。本研究结果为进一步了解脓毒症诱导的血管损伤分子机制提供了新的实验依据。

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