Figure 7.

Exogenous tumor necrosis factor (TNF)-α counteracts the effects of SEM18 peptide. (A) Binding of TNF-α to TNF receptor 1, as measured at 24 h after lipopolysaccharide (LPS) administration using immunofluorescence staining of proximity ligation assay (PLA). (B) Plasma concentrations of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and the wet/dry (W/D) weight ratio of the liver tissues, as measured at 24 h after LPS administration. (C) The quantitative sum intensity of phosphorylated mixed lineage kinase domain-like pseudokinase (p-MLKL), nod-like receptor protein 3 (NLRP3), and microtubule-associated protein 1A/1B-light chain 3 (LC3) in liver tissues, as measured at 24 h after LPS administration using immunohistochemistry staining assay. For apoptosis analysis, liver tissues were assayed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) method and the mean TUNEL-positive cell in liver tissues (per 0.25 mm²) was calculated, as measured at 24 h after LPS administration. LPS: the LPS (15 mg/kg) group; LSEM: the LPS (15 mg/kg) plus SEM18 peptide group; LSEM + TNF-α: the LPS (15 mg/kg) plus SEM18 peptide and TNF-α group. Data are the mean ± standard deviation. Data of PLA, plasma ALT and AST, W/D weight ratio, immunohistochemistry staining assay, and TUNEL assay were derived from five, four, four, four, and four mice from each group, respectively. ^# p < 0.05, the LSEM group vs. the LPS group; ^† p < 0.05, the LSEM + TNF-α group vs. the LSEM group.