Zuohua Xie1, Bing Lin1, Xinju Jia1, Ting Su1, Ying Wei1, Jiping Tang1, Chengzhi Yang2, Chuanbao Cui3, Jinxiang Liu4. 1. Department of Critical Care Medicine, The Third Affiliated Hospital of Guangxi Medical University, Nanning, PR China. 2. Graduate School, Guangxi Medical University, Nanning, PR China. 3. Department of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, PR China. 4. Department of Critical Care Medicine, The Third Affiliated Hospital of Guangxi Medical University, Nanning, PR China. 13977128063@139.com.
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.
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.
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