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
日期:2021-11-01
卷期号:36 (11): 1179-1187
被引量:4
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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