Fig. 1: LPS-induced significant upregulation of LCN2.
From: LCN2 induces neuronal loss and facilitates sepsis-associated cognitive impairments
A Heatmap illustrating the expression levels of differentially expressed genes (DEGs) identified in dataset GSE88959. B Volcano plot of DEGs in GSE88959. Genes with |Log2FoldChange| > 5 are highlighted. C Venn diagram illustrates the intersection between DEGs (|Log2FoldChange| > 2 and P < 0.05) and core enrichment genes in the “Immune system” pathways (Reactome). D Protein-Protein Interaction (PPI) network of intersected genes, highlighting LCN2, CD244, MMP3, FCGR3A, and MNDA as hub genes. Size represents Log2FoldChange. E Brain tissues (hippocampus) from the two groups were homogenized and LCN2 levels were detected by immunoblotting. Actin was used as a loading control. F Quantitative analysis of LCN2 levels (n = 4). G Representative immunofluorescence images show GFAP and LCN2 fluorescence in brain slices of two groups. H Quantitative analysis of GFAP and LCN2 fluorescence in hippocampal slices, (n = 4). I Representative immunofluorescence images show GFAP and LCN2 fluorescence in primary hippocampal astrocytes. J Quantitative analysis of LCN2 fluorescence in primary hippocampal astrocytes (n = 9–10). K GFAP and LCN2 protein levels were detected in primary hippocampal astrocytes by immunoblotting, actin were used as a loading control. Quantitative analysis of the GFAP (L) and LCN2 (M), (n = 4). N ELISA kit was used to measure the LCN2 levels in ACM, (n = 4). Data are presented as Mean ± SEM. A non-parametric test of Mann-Whitey test was used for statistical analysis in (F, H, L, M, N). A two-tailed Student’s t-test was used for statistical analysis in statistical analysis in (J).*p < 0.05, ****p < 0.0001, versus Control group.
