cox2  (Proteintech)

Journal: Regenerative Therapy

Article Title: Hypoxia-preconditioned bone marrow mesenchymal stem cell-derived exosomes ameliorate knee osteoarthritis by promoting cartilage regeneration and alleviating pain in rats

doi: 10.1016/j.reth.2025.101049

Figure Lengend Snippet: Hypo-BMSCs-Exos attenuate IL-1β-Induced Chondrocyte Inflammation. A: Immunofluorescence staining reveals changes in iNOS, and COX2 in IL-1β-induced chondrocytes following intervention with Norm-BMSCs-Exos and Hypo-BMSCs-Exos. B: Quantitative analysis of immunofluorescence staining. C: Western blot detection of protein expression levels of iNOS, and COX2 in IL-1β-induced chondrocytes treated with Norm-BMSCs-Exos and Hypo-BMSCs-Exos. D: Statistical analysis of relative protein band intensity values. Data are presented as Mean ± SD. Intergroup differences with statistical significance: ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, n = 3 per group.

Article Snippet: The sections were blocked with 10 % fetal bovine serum (FBS) for 1 h at room temperature, then incubated overnight at 4 °C with primary antibodies against iNOS (Servicebio, China), COX2 (ProteinTech Group, China), Collagen II (Bioss, China), aggrecan (Bioss, China), MMP-13 (ProteinTech Group, China), and ADAMTS-5 (Zenbio, China).

Techniques: Immunofluorescence, Staining, Western Blot, Expressing

Journal: Regenerative Therapy

Article Title: Hypoxia-preconditioned bone marrow mesenchymal stem cell-derived exosomes ameliorate knee osteoarthritis by promoting cartilage regeneration and alleviating pain in rats

doi: 10.1016/j.reth.2025.101049

Figure Lengend Snippet: Intra-articular injection of Hypo-BMSCs-Exo protects articular cartilage from degeneration in KOA rats. A: Representative images of immunohistochemical staining for iNOS, COX2, Collagen II, Aggrecan, ADAMTS-5, and MMP-13 in cartilage tissue at 8 weeks post-intervention. Scale bar = 50 μm. B: Quantitative analysis and statistical evaluation of immunopositive cells. Data are expressed as mean ± standard deviation (SD), with n = 3 per group. Intergroup statistical significance is indicated as: ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared to control rats; # p < 0.05、 ## p < 0.01、 ### p < 0.001 indicate differences compared with OA rats; & p < 0.05、 && p < 0.01、 &&& p < 0.001 indicate differences compared with Norm-BMSCs-Exos rats.

Article Snippet: The sections were blocked with 10 % fetal bovine serum (FBS) for 1 h at room temperature, then incubated overnight at 4 °C with primary antibodies against iNOS (Servicebio, China), COX2 (ProteinTech Group, China), Collagen II (Bioss, China), aggrecan (Bioss, China), MMP-13 (ProteinTech Group, China), and ADAMTS-5 (Zenbio, China).

Techniques: Injection, Immunohistochemical staining, Staining, Standard Deviation, Control

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: