Cedrol ameliorates ulcerative colitis via myeloid differentiation factor 2-mediated inflammation suppression, with barrier restoration and microbiota modulation

Figure 6 Cedrol inhibited toll-like receptor 4-mediated mitogen-activated protein kinase and nuclear factor kappa B signaling in vivo and in vitro. A-D: Phosphorylated and total protein abundance of mitogen-activated protein kinase signaling molecules [extracellular regulated protein kinase (ERK)1/2, c-Jun N-terminal kinase (JNK), p38] in colonic tissues of mice (n = 6); E: Cellular viability was quantified with the cell counting kit-8 method (n = 3); F-H: Proinflammatory cytokine expression in RAW264.7 macrophages across experimental groups (n = 3); I-K: Inducible nitric oxide synthase and cyclooxygenase-2 protein expression in RAW264.7 cells across groups (n = 3); L-P: Phosphorylated and total protein expression of ERK1/2, JNK, p38 and nuclear factor kappa B p65 in RAW264.7 macrophages (n = 3). Data are expressed as mean ± SD. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. ^dP < 0.0001. CE: Cedrol; DSS: Dextran sulfate sodium; ERK: Extracellular regulated protein kinase; p-ERK: Phospho-extracellular regulated protein kinase; JNK: C-Jun N-terminal kinase; p-JNK: Phospho-c-Jun N-terminal kinase; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; TNF: Tumor necrosis factor; IL: Interleukin; mRNA: Messenger RNA; LPS: Lipopolysaccharide; iNOS: Inducible nitric oxide synthase; COX-2: Cyclooxygenase-2.