Effect of Insulin on Lipopolysaccharide-Induced Inflammatory Response in MLE-12 Cells
Objective To study the molecular mechanism of insulin attenuating the inflammatory response of lipopolysaccharide on mouse lung epithelial cells by detecting the expression of TNF-α,TLR4,AKT and ERK in the lipopolysaccharide-induced inflammatory model of MLE-12 cells,with a view to providing exper-imental basis and theoretical basis for potential therapeutic approaches for acute lung injury.Methods MLE-12 cells were used as the research object,induced by adding lipopolysaccharide(10 ug/ml)for 24h,to construct the model of inflammatory alveolar epithelial cell injury,replacing the serum medium,and treated with insulin or PBS for 72h.The cells were divided into 5 groups:control group(C):MLE-12 cells were cultured in regular medium;LPS group(L):MLE-12 cells were cultured by adding LPS(10 ug/ml);LPS+Insulin 1 group(L+I1):which 0.1 nM insulin treatment was added to continue the culture;LPS+Insulin 2 group(L+I2):which 1nM insulin treatment was added to continue the culture;LPS+insulin 3 group(L+I3):which 3nM in-sulin treatment was added to continue the culture.Each group was measured at three time points,12h,24h and 72h,respectively.Results The expression of cellular inflammatory factors such as TNF-α and TLR4 was sig-nificantly elevated in MLE-12 cells in the presence of lipopolysaccharide(10 ug/ml).Treatment with insulin partially inhibited the inflammatory response caused by lipopolysaccharide on MLE-12 cells.Insulin can reduce the inflammatory response in lung epithelial cells by inhibiting the phosphorylation levels of proteins in the PI3K/AKT and MAPK/ERK signaling pathways.Conclusion Insulin attenuates the inflammatory response of lipopolysaccharide on alveolar epithelial cells in part by regulating the levels of AKT and ERK phosphorylation.This provides a preliminary theoretical basis for the rational clinical application of insulin intervention in the treatment of ALR/ARDS.
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