Skip to main content
Fig. 3 | Journal of Translational Medicine

Fig. 3

From: Monophosphoryl lipid A ameliorates radiation-induced lung injury by promoting the polarization of macrophages to the M1 phenotype

Fig. 3

MPLA promoted the proliferation of MLE-12 cells by activating TLR4 on macrophages to trigger the production of exosomes. A, Survival fraction of MLE-12 cell at different MPLA concentrations. B, The level of TLR4 in tissues from various lung cancer patients and normal tissues. Data were obtained from the TCGA and GTEx databases. C, The TLR4 expression detected after MPLA treatment in MLE-12 cells, Beas-2B cells and RAW 264.7 cells. D, Protein levels of TLR4 as determined by western analysis in MLE-12 cells, Beas-2B cells and RAW 264.7 cells at different times after irradiation. E, H, The colony-forming ability of MLE-12 cells exposed to different IR radiations. F, I, The “multi-target-single-hit-model” for determining the cell viability of MLE-12 cells. G, Top 10 enriched biological processes, molecular functions, cellular components of TLR4 in data obtained from the TCGA database. *P < 0.05, **P < 0.01, *** P < 0.001,****P < 0.0001

Back to article page