Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

Figure 8 NaCl promotion of inflammation relies on the p38/MAPK pathway. A: LPMCs were stimulated with 60 mmol/L NaCl in the presence of 100 ng/mL LPS and 20 ng/mL IFN-γ for 1 h, 6 h, 12 h and 24 h, and the p38 and phosphorylated-p38 proteins were detected by western blot; B: LPMCs were stimulated with different NaCl concentrations in the presence of 100 ng/mL LPS and 20 ng/mL IFN-γ for 24 h and phosphorylated p38 protein was detected by western blot; C: LPMCs were stimulated with different NaCl concentrations in the presence of LPS and IFN-γ, and the mRNA expression of SGK1 was measured by RT-PCR; D: LPMCs were pretreated with 10 μmol/L SB or DMSO for 2 h and were subsequently stimulated with 60 mmol/L NaCl along with 100 ng/mL LPS and 20 ng/mL IFN-γ in the presence of DMSO or 10 μmol/L SB for 24 h and the proteins of p38 and phosphorylated-p38 were detected by western blot. In all the panels, data indicate three separate experiments. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. DSS: Dextran sulfate sodium; LMPCs: Lamina propria mononuclear cells; LP: Lamina propria; LPS: Lipopolysaccharide; MLN: Mesenteric lymph node; SB: SB20358; SP: Spleen.