Journal: Pharmaceuticals

Article Title: Scutellarein from Erigeron breviscapus Inhibits Apoptosis-Mediated Epithelial Barrier Disruption and Alleviates Cigarette Smoke-Induced Lung Injury

doi: 10.3390/ph19010113

Figure Lengend Snippet: Scu reduces CS-induced inflammatory responses in BALF and lung tissue. Quantification of leukocytes ( A ), neutrophils ( B ), lymphocytes ( C ), and monocytes ( D ) in BALF from FA or CS-exposed mice receiving Veh (0.3% ( w / v ) CMC-Na solution containing 0.2% ( v / v ) Tween-80 and 0.2% ( v / v ) DMSO), 5, 10, 15 mg/kg Scu or 5 mg/kg Dex. Quantification of the contents of IL-1β ( E ), CXCL1 ( F ), TNF-α ( G ), and MCP-1 ( H ) in BALF from mice treated as in ( A – D ). Relative mRNA expression levels of Il1b ( I ), Cxcl1 ( J ), Tnf ( K ), Mcp-1 ( L ), and Mmp-9 ( M ) in lung tissue samples collected from differently treated mice. ( N ) Quantification of myeloperoxidase (MPO) in lung tissue samples collected from differently treated mice. Data represent mean ± SEM. N = 6; *, p < 0.05, **, p < 0.01, vs. FA-Veh; #, p < 0.05, ##, p < 0.01, vs. CS-Veh, by one-way ANOVA with Bonferroni’s multiple comparisons tests.

Article Snippet: ELISA kit of IL-1β (Cat# E-EL-M0037), TNF-α (Cat# E-EL-M3063), CXCL1 (Cat# E-EL-M0018), MCP1 (Cat# E-EL-M3001) were purchased from Elabscience Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Expressing

Journal: Pharmaceuticals

Article Title: Scutellarein from Erigeron breviscapus Inhibits Apoptosis-Mediated Epithelial Barrier Disruption and Alleviates Cigarette Smoke-Induced Lung Injury

doi: 10.3390/ph19010113

Figure Lengend Snippet: Scu significantly alleviates CSC-induced pulmonary epithelial inflammation and barrier damage. Relative mRNA levels of Il1b ( A ), Cxcl1 ( B ), Tnf ( C ), Mcp-1 ( D ), and Mmp-9 ( E ) in MLE-12 cells treated with CSC for 12 h with or without Scu (1 μM) co-treatment. Data were expressed relative to the Veh. ( F ) Representative fluorescent images of MLE-12 cells stained with ZO-1, E-cadherin, Occludin, Claudin-18 (green), and Hoechst 33342 (blue) after being exposed to Veh (0.1% DMSO) or CSC (50 μg/mL) for 12 h with or without Scu (1 μM) co-treatment. Scale bar = 5 μm. ( G ) Changes in the TEER values of MLE-12 cell monolayer receiving Veh (0.1% DMSO) or CSC (50 μg/mL) treatment for 12 h with or without Scu (1 μM) co-treatment. ( H ) Changes in the Pd value of MLE-12 cells receiving Veh or CSC (50 μg/mL) for 12 h with or without Scu (1 μM) co-treatment. Data represent mean ± SEM. N = 6; **, p < 0.01, vs. Veh; #, p < 0.05, ##, p < 0.01, vs. CSC, by one-way ANOVA with Bonferroni’s multiple comparisons tests.

Article Snippet: ELISA kit of IL-1β (Cat# E-EL-M0037), TNF-α (Cat# E-EL-M3063), CXCL1 (Cat# E-EL-M0018), MCP1 (Cat# E-EL-M3001) were purchased from Elabscience Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Staining

Journal: British Journal of Cancer

Article Title: Interleukin-8 and its receptor CXCR2 in the tumour microenvironment promote colon cancer growth, progression and metastasis

doi: 10.1038/bjc.2012.177

Figure Lengend Snippet: Proliferation of CT26 and HCT116 cancer cells was activated by the IL-8 and CXCR2 pathway. ( A – D ) IF images of CXCR2 on CT26 ( A ) and HCT116 ( C ) cancer cell lines. The same IF assays were performed without the primary antibody to confirm the specificity of the primary antibody for CXCR2 ( B , D ). Bar, 20 μ m. ( E , F ) Proliferation assays were performed on CT26 ( E ) or HCT116 ( F ) cells in a low serum (1%) media containing vehicle (DMSO), hIL-8 (10 ng ml −1 ) or Gro- α (10 ng ml −1 ). ( G , H ) The CXCR2 antagonist, SCH-527123, efficiently blocked the IL-8-induced activation of cell proliferation. Proliferation assay was performed with vehicle (DMSO), or IL-8 (10 ng ml −1 ) in the presence of SCH-527123 (10 or 25 μ M ) on CT26 ( G ) and HCT116 ( H ) cells. SCH, SCH-527123. Data are expressed as mean±s.d.; * P <0.05; ** P <0.005.

Article Snippet: In addition to IL-8, CXCR2 can be activated by other cytokines such as Gro- α /CXCL1, which has been also adversely associated with colon cancer development and progression ( Cuenca et al , 1992 ; Baier et al , 2005 ; Wen et al , 2006 ; Ogata et al , 2010 ).

Techniques: Activation Assay, Proliferation Assay