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[This corrects the article DOI: 10.1016/j.apsb.2021.11.009.].
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Objective To investigate the influence of proinflammatory factor interleukin-18(IL-18) on vein endothelial cell function by activating NF-κB mediated cell signal pathway and its association with deep vein thrombosis(DVT).Methods Recombinant human IL-18 was used to act on in vitro cultured human umbilical vein endothelial cell(HUVECs).The NF-κB activation inhibitor was used to conduct interference.The detection measures of real time fluorescence quantitative PCR,Western blot,immunofluorescence and flow cytometry were used to verify whether IL-18 affect the expression of endothelial cellular function markers such as HUVECs normal statusand vWF,P-selectin and tissue plasminogen activator(t-PA) by activating NF-κB mediated cell signal pathway.Moreover the mechanism of IL-18 participating in the DVT was performed the comprehensive analysis by combining with previous study.Results IL-18 could activate NF-κB in endothelial cell,increased the p65 expression in nucleus,decreased the intracellular IκBα expression and significantly increased early apoptosis cells in HUVECs;adding QNZ(EVP4593) could significantly inhibit the activation effect of IL-18 on NF-κB,the occurrence of cellular injury and apoptosis was significantly reduced;IL-18 could promote the abnormal expression of DVT related endothelial cell markers vWF,P-selectin and t-PA (P<0.05).But various markers could recover conventional expression after inhibiting NF-κB activation.Conclusion The interaction between Il-18 and NF-κB causes the abnormality of HUVECs growth status and function,which may be the DVT onset related pathogenic mechanism.
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Objective To investigate the correlation between IL‐18 and deep venous thrombosis disease and its clinical significa‐tion .Methods To detect the expression of IL‐18 by ELISA ,we collected the blood samples of DVT patients as the experimental group(n=40) compared to the control group(n=40) and normal group(n=20) .IL‐18 over expression/interference vectors were constructed and transfected human vein endothelial cells ,analyzed by microarray and KEGG Pathway as biology information tech‐nology .Then discuss the association between IL‐18 and DVT .Results Results of ELISA showed that compared with control group and normal group ,the expression of IL‐18 gene in DVT patient were up‐regulated(F=11 .248 ,P0 .05) .Immunofluorescence detected IL‐18 gene expression in cytoplasm of human umbilical vein endothelial cells (HUVECs) .According to the microarray analysis we found in the IL18‐pCDH‐GFP transfected cells 17 signaling pathways were down‐expressed while 16 signaling pathways were up‐expressed .Compared with normal group cells ,in the IL18‐LMP‐shRNAmir1 transfected cells 23 signaling pathways were down‐ex‐pressed and 9 signaling pathways were up‐expressed .Conclusion Based on the above experimental data ,it is very clear that IL‐18 influenced HUVECs and plays an important role in DVT ,it is possible to predict the diagnosis of DVT and act as candidate molecu‐lar markers .
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Objective To investigate the association between the signaling pathways of MCP-1-pCDH-GFP-trans?fected cells and deep venous thrombosis (DVT). Methods The cultured human umbilical vein endothelial cells (HUVECs) were tested by immunofluorescence and co-immunoprecipitation methods. The constructed MCP-1 over-expression/interfer?ence vector, and the change of transcription profile were detected by microarray assay and biological information technology analysis. Results MCP-1 over-expression/interference vector MCP-1-pCDH-GFP/MCP-1-LMP shRNAmir1 was con?structed and HUVECs were transfected. According to the microarray analysis we found that there were 18 down-expressed signaling pathways and 7 up-expressed signaling pathways in MCP-1-pCDH-GFP-transfected cells. There were 60 down-expressed signaling pathways and 15 up-expressed signaling pathways in the MCP-1-LMP shRNAmir1 transfected cells. Conclusion Signaling pathways of MCP-1 plays an important role in DVT formation,which may provide us a new way to study molecular mechanism of DVT.
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Objective To build rat DVT inferior vena cava partial stasis (narrow) model, to detected the expression ofβ2-GP1, VEGF and TF in rat blood, and to investigat the correlation betweenβ2-GP1, VEGF and TF with DVT. Meth?ods SD rats (n=70) are divided into control group (n=10), sham operation group (n=30) and the model group (n=30) ran?domly and DVT model was built by the inferior vena cava partial stasis (narrow) after 2 h, 8 h and 24 h respectively. In each time point, ten rats were taken in each group, inferior vena cava blood were collected whileβ2-GP1, VEGF and TF expres?sion were detected by ELISA. Results In rat experiment, compared with control group, there was no significant change in?expression of β2-GP1, VEGF and TF in sham operation group (P > 0.05). Levels of β2-GP1, VEGF and TF were in?creased at the 2nd hour and 8th hour then peak at the 24th hour which was higher than those in the 24th hour control group and in Sham group and it was also higher than those in the 2nd hour and the 8th hour in model group with statistical signifi?cant difference (P<0.01). Conclusion Based on the above experimental data, in rat DVT formation process, β2-GP1, VEGF and TF may play an important role in promote DVT formation.
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Objective To investigate the effect of Helicobacter pylori (Hp) infection on macrophage migration inhibitory factor (MIF) protein expression and explore the role of Hp and MIF in the development of chronic gastritis and gastric ulcer. Methods The biopsy tissues of gastric mucosa were collected under gastroscope, and Hp was detected by 14C breath test and Warthin-starry method. We recruited 25 healthy people with normal gastric mucosa, 40 patients pathologically confirmed Hp-positive with chronic superficial gastritis, 40 with atrophic gastritis and 40 with gastric ulcer. MIF protein expression was examined by immunohistochemical SP staining method, then Hp eradication was performed on Hp-infected chronic superficial gastritis, atrophic gastritis and gastric ulcer for 2 weeks. Hp and MIF were re-examined 4 weeks after drug withdrawal, and difference in MIF expression was compared between Hp-infected patients and Hp-eradicated patients. Results The expression of MIF was low in normal gastric mucosa without Hp infection (2/25, 8%), but significantly higher in Hp-infected gastric mucosa with chronic superficial gastritis (12/40, 30%), atrophic gastritis (26/40, 65%) and gastric ulcer (19/40, 47.5%); there was a significant difference between normal gastric mucosa without Hp infection and that of comHp-infected patients (57/120 vs. 2/25; χ~2=13.376, P<0.01). MIF expression increased with the severity of inflammation in chronic gastritis, and there was a significant difference between superficial gastritis and atrophic gastritis (12/40 vs. 26/40; χ~2=9.825, P<0.01). The expression of MIF was noticeably decreased after Hp eradication compared with before(57/120 vs. 23/103; χ~2=15.264, P<0.01); however, there was no significant change in those patients whose Hp was still positive. Conclusion The expression of MIF on gastric mucosa is associated with the development of chronic gastritis and gastritis ulcer caused by Hp infection. Eradication of Hp could cut down the abnormally high MIF expression in gastric mucosa and slow down the formation and development of gastric carcinoma.