Journal: World Journal of Gastroenterology

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

doi: 10.3748/wjg.v32.i2.114057

Figure Lengend Snippet: 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. a P < 0.05. b P < 0.01. c P < 0.001. d P < 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.

Article Snippet: After blocking in 5% skim milk, membranes were incubated overnight at 4 °C with primary antibodies targeting: Phospho-extracellular regulated protein kinase (ERK) 1/2 (Thr202/Tyr204); ERK1/2; Phospho-c-Jun N-terminal kinase (JNK) (Thr183/Tyr185); JNK; Phospho-p38 (Thr180/Tyr182); P38, phospho-nuclear factor kappa B (NF-κB) p65 (Ser536); NF-κB p65 (Cell Signaling Technology, Daners, MA, United States); Cyclooxygenase-2 (COX-2); Inducible nitric oxide synthase (iNOS); Glyceraldehyde-3-phosphate dehydrogenase (Proteintech, Wuhan, Hubei Province, China).

Techniques: In Vivo, In Vitro, Quantitative Proteomics, Cell Counting, Expressing

Journal: World Journal of Gastroenterology

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

doi: 10.3748/wjg.v32.i2.114057

Figure Lengend Snippet: Cedrol treated dextran sulfate sodium-induced colitis by inhibiting inflammation, restoring the intestinal barrier, and rebalancing gut microbiota. TNF: Tumor necrosis factor; IL: Interleukin; DSS: Dextran sulfate sodium; LPS: Lipopolysaccharide; MD2: Myeloid differentiation factor 2; TLR4: Toll-like receptor 4; MAPK: Mitogen-activated protein kinase; ERK: Extracellular regulated protein kinase; JNK: C-Jun N-terminal kinase; NF-κB: Nuclear factor kappa B; iNOS: Inducible nitric oxide synthase; COX-2: Cyclooxygenase-2.

Article Snippet: After blocking in 5% skim milk, membranes were incubated overnight at 4 °C with primary antibodies targeting: Phospho-extracellular regulated protein kinase (ERK) 1/2 (Thr202/Tyr204); ERK1/2; Phospho-c-Jun N-terminal kinase (JNK) (Thr183/Tyr185); JNK; Phospho-p38 (Thr180/Tyr182); P38, phospho-nuclear factor kappa B (NF-κB) p65 (Ser536); NF-κB p65 (Cell Signaling Technology, Daners, MA, United States); Cyclooxygenase-2 (COX-2); Inducible nitric oxide synthase (iNOS); Glyceraldehyde-3-phosphate dehydrogenase (Proteintech, Wuhan, Hubei Province, China).

Techniques:

Journal: Frontiers in Pharmacology

Article Title: Cinnamomum verum extract as a potential therapeutic for atopic dermatitis through reducing lipid peroxidation and oxidative stress

doi: 10.3389/fphar.2025.1714816

Figure Lengend Snippet: CVE inhibits NF-κB activation and pro-inflammatory protein expression through ALDH2 activation. (A) ALDH2 expression levels were analyzed by Western blotting in HaCaT cells treated with TNF-α/IFN-γ and CVE. (B) NF-κB pathway activation was assessed by analyzing the phosphorylation levels of IκBα and p65 by Western blotting in HaCaT cells treated with TNF-α/IFN-γ and CVE. (C) COX-2 and iNOS expression levels were evaluated by Western blotting in HaCaT cells treated with TNF-α/IFN-γ and CVE. Data represent the mean ± SEM. ### p < 0.001 vs. untreated control. ** p < 0.01; *** p < 0.001 vs. TNF-α/IFN-γ -treated group.

Article Snippet: Proteins were then transferred to a polyvinylidene fluoride membrane (GVS filter technology, Sanford, Maine, United States) and blocked in 5% Bovine Serum Albumin in Tris-Buffered Saline (TBS) containing 0.1% Tween-20 (TBS-Tween; WB) for 2 h. After blocking, proteins were incubated with an appropriate primary antibody ALDH2 (#ATGA0450, NKMAX, Seoul, Republic of Korea), p-NF-κB (#3031, Cell Signaling Technology, MA Danvers, United States), p-IκBα (#2859, Cell Signaling Technology, MA Danvers, United States), COX-2 (#12282, Cell Signaling Technology, MA Danvers, United States), iNOS (#13120, Cell Signaling Technology, MA Danvers, United States), and β-actin (#ATGA0570, NKMAX, Seoul, Republic of Korea) overnight at 4 °C.

Techniques: Activation Assay, Expressing, Western Blot, Phospho-proteomics, Control

Journal: Frontiers in Pharmacology

Article Title: Cinnamomum verum extract as a potential therapeutic for atopic dermatitis through reducing lipid peroxidation and oxidative stress

doi: 10.3389/fphar.2025.1714816

Figure Lengend Snippet: Schematic illustration of the CVE was evaluated using in vitro keratinocytes, in vivo SKH-1 mice. CVE attenuated atopic dermatitis (AD) by suppressing oxidative stress and NF-κB-mediated inflammatory signaling, reducing inflammatory mediators, and regulating lipid peroxidation-derived 4-hydroxynonenal (4-HNE). These results enhanced cellular antioxidant capacity, increased ALDH2 expression, and decreased lipid peroxidation and inflammation, ultimately ameliorating AD symptoms.

Article Snippet: Proteins were then transferred to a polyvinylidene fluoride membrane (GVS filter technology, Sanford, Maine, United States) and blocked in 5% Bovine Serum Albumin in Tris-Buffered Saline (TBS) containing 0.1% Tween-20 (TBS-Tween; WB) for 2 h. After blocking, proteins were incubated with an appropriate primary antibody ALDH2 (#ATGA0450, NKMAX, Seoul, Republic of Korea), p-NF-κB (#3031, Cell Signaling Technology, MA Danvers, United States), p-IκBα (#2859, Cell Signaling Technology, MA Danvers, United States), COX-2 (#12282, Cell Signaling Technology, MA Danvers, United States), iNOS (#13120, Cell Signaling Technology, MA Danvers, United States), and β-actin (#ATGA0570, NKMAX, Seoul, Republic of Korea) overnight at 4 °C.

Techniques: In Vitro, In Vivo, Derivative Assay, Expressing