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

细胞凋亡 败血症 流式细胞术 车站3 免疫学 肿瘤坏死因子α 白细胞介素 污渍 脂多糖 细胞生长 医学 细胞因子 癌症研究 男科 生物 生物化学 基因
作者
Zuohua Xie,Bangjiang Lin,Xin Jia,Ting Su,Ying Wei,Jiping Tang,Chengzhi Yang,Chuanbao Cui,Jinxiang Liu
出处
期刊:PubMed 卷期号:36 (11): 1179-1187 被引量:4
标识
DOI:10.14670/hh-18-375
摘要

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.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.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.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.

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