Effect of MCP-1 gene on occurrence of acute kidney injury(AKI)in sepsis
Objective To investigate the effect of monocyte chemoattractant protein-1(MCP-1)gene on sepsis induced acute kidney injury(AKI).Methods 50 patients with sepsis AKI admitted to the hospital from September 2022 to September 2023 were selected as AKI group,and 50 healthy subjects in the same period were included as control group.5 mL fasting venous blood was collected from all subjects in the morning,and the expression of MCP-1 in the serum of AKI patients and healthy people was detected by ELISA.The primary cultured renal tubular epithelial cells were identified by immunofluorescence using CK14 and CK18 antibodies.MCP-1 gene was over-expressed and interfered.The cell proliferation assay kit and RT-qPCR were used to detect the proliferation of renal tubular epithelial cells and the changes in the expression of inflammatory factors,including tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin-6(IL-6),interleukin-10(IL-10)and γ-interferon(IFN-γ).Results Compared with con-trol group,the expression of MCP-1 in peripheral blood and urine of AKI group was significantly increased(P＜0.05).According to the identification of cellular immunofluorescence,the epithelial cell markers CK14 and CK18 were selected.When cultured for 24 hours,more than 90％of the cells expressed the cell marker CK18,and about 84％of the cells expressed CK14.Compared with NC group,the number of cells in siRNA group were increased at 24 and 48 hours(P＜0.05).Compared with MCP-1 group,the number of cells in siRNA group were increased at 24,48 and 72 hours(P＜0.05).The expression levels of IL-1β,IL-6 and IFN-y in NC group were increased gradually with the passage of time.The expression levels of IL-1β,IL-6,IL-10,IFN-γ and TNF-α in MCP-1 group were increased gradually with the passage of time.The expression levels of IL-1β,IL-6 and IFN-γ were no significant upward trend in siRNA group.Conclu-sion MCP-1 gene may play an important role in the pathogenesis of sepsis induced AKI,which may regu-late IL-1β and other inflammatory cytokines to inhibit the growth and proliferation of renal tubular epithe-lial cells,thus participating in the process of AKI in patients with sepsis.
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