Skip to main content
. 2020 Sep 29;13(10):280. doi: 10.3390/ph13100280

Figure 3.

Figure 3

SEM18 peptide mitigates tumor necrosis factor (TNF)-α binding to TNF receptor 1 (TNFR1) and decreases liver injury induced by endotoxin. (A) Binding of TNF-α to TNFR1 in liver tissues, as measured at 24 h after lipopolysaccharide (LPS) or normal saline (NS) administration using immunofluorescence staining of proximity ligation assay (PLA). Red dots: positive PLA signal showing protein–protein interactions between TNF-α and TNFR1 in liver tissues. Blue dots: DAPI (4′,6-diamidino-2-phenylindole) stain showing a cell nucleus in liver tissues. (B) Representative microscopic findings of the liver tissues stained with hematoxylin–eosin (200×) and the organ injury scores (Suzuki’s scores), as measured at 24 h after LPS or NS administration. (C) Plasma concentrations of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), as measured at 24 h after LPS or NS administration. Sham: the NS group; SEM: the NS plus SEM18 peptide group; CP: the NS plus control peptide (CP) group; LPS: the LPS (15 mg/kg) group; LSEM: the LPS (15 mg/kg) plus SEM18 peptide group; LCP: the LPS (15 mg/kg) plus CP group. Data are presented as the mean ± standard deviation. Data related to PLA, microscopic findings, Suzuki’s score, AST, and ALT were derived from five, five, six, and six mice from each group, respectively. * p < 0.05, the LPS group vs. the sham group; # p < 0.05, the LSEM group vs. the LPS group; † p < 0.05, the LCP group vs. the LSEM group.