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Image Search Results
Journal: Journal of Applied Biological Chemistry
Article Title: Phenolic compounds from the flowers of Cosmos bipinnatus and their anti-atopic activity
doi: 10.3839/jabc.2022.028
Figure Lengend Snippet: Fig. 4 TARC assay using compound 1 and 2 from the flowers of Cosmos bipinnatus. TARC assay of samples were performed in concentration dependent manner. Results are presented as mean ± SEM. *p ≤0.05, **p ≤0.01, ***p ≤0.001 compared with control. Dexa: dexamethasone (positive control)
Article Snippet:
Techniques: Concentration Assay, Control, Positive Control
Journal: The Journal of Experimental Medicine
Article Title: Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation
doi: 10.1084/jem.20110522
Figure Lengend Snippet: Local chemokines induce NKT cell extravasation. (A) Chemokine messenger RNA expression profile of total lungs from WT or CD1d −/− mice 18 h after airway exposure to saline or PBS57 as indicated. Data were normalized to control unmanipulated WT mice, with bars showing the mean ± SEM of two independent experiments. Shown are ccl1 (01), ccl2 (02), ccl3 (03), ccl4 (04), ccl5 (05), ccl6 (06), ccl7 (07), ccl8 (08), ccl9 (09), ccl11 (10), ccl12 (11), ccl17 (12), ccl19 (13), ccl20 (14), ccl21 (15), ccl22 (16), ccl24 (17), ccl25 (18), ccl27a (19), ccl28 (20), cxcl1 (21), cxcl2 (22), cxcl3 (23), pf4/cxcl4 (24), cxcl5 (25), ppbp/cxcl7 (26), cxcl9 (27), cxcl10 (28), cxcl11 (29), cxcl12 (30), cxcl13 (31), cxcl14 (32), cxcl15 (33), cxcl16 (34), cxcl17 (35), cx3cl1 (36), and xcl1 (37). IT, intratracheal. (B) Time course of protein expression of CCL17 (TARC), CXCL9 (MIG), and CXCL13 (BLC) in total lung lysates after intratracheal exposure to PBS57. Data are representative of two separate experiments with two to three individual mice analyzed at each time point. (C) NKT cell extravasation 48 h after intratracheal administration of 100 ng CCL17 was measured by the absolute number of lung tetramer + cells that were protected from a 2-min intravascular anti–CD45-PE labeling. EdU incorporation after a 3-h pulse was <1% in all groups (not depicted). (B and C) Horizontal bars indicate the mean. *, P < 0.05; ***, P < 0.001.
Article Snippet: CCL17 was also independently measured using the
Techniques: RNA Expression, Saline, Control, Expressing, Labeling
Journal: Frontiers in Pharmacology
Article Title: Hybrid Cannabis sativa L. inflorescences exert an anti-inflammatory effect through the modulation of MAPK/NF-κB/NLRP3 inflammasome and JAK1/STAT6 pathway in HaCaT cells
doi: 10.3389/fphar.2025.1617180
Figure Lengend Snippet: Inhibitory effect of HCIE on AD-related cytokines expression in HaCaT cells. Gene expression of AD-related cytokines was measured using RT-PCR. The cells were pre-treated with the indicated concentrations of HCIE for 30 min and stimulated with TNF-α/IFN-γ (each 10 ng/mL). The relative mRNA levels of (A) IL-4, (B) IL-13, (C) MDC, (D) RANTES, (E) TARC, and (F) CXCL10 were measured, and mRNA was normalized to GAPDH. Secreted (G) RANTES and (H) TARC were evaluated using ELISA. (I) The percentage of relative gene expression was calculated. Data represented as mean ± SD ( n = 3) and the p values are presented on the graph as follows: ### p < 0.001 vs control group; ** p < 0.01, and *** p < 0.001 vs TNF-α/IFN-γ induced group.
Article Snippet: For the measurement of secreted cytokines, the RANTES ELISA kit (#DY278-05; R&D Systems, Minneapolis, MN, United States) and
Techniques: Expressing, Gene Expression, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Control
Journal: American Journal of Cancer Research
Article Title: Chemokine CCL17 induced by hypoxia promotes the proliferation of cervical cancer cell
doi:
Figure Lengend Snippet: Cervical cancer cells express a high level of CCL17. A. Immunohistochemistry analysis for CCL17 expression in cervical cancer (n=10). Original magnification: ×400. B. The secretion level of CCL17 from HeLa (3×105 cells/well) and SiHa cells (3×105 cells/well) after culture for 24 h or 48 h. The data are expressed as the mean ± SD. *P<0.05, **P<0.01 and ***P<0.01 (one-way ANOVA).
Article Snippet: And the secretion level of CCL17 in the culture supernatant was analyzed by
Techniques: Immunohistochemistry, Expressing
Journal: American Journal of Cancer Research
Article Title: Chemokine CCL17 induced by hypoxia promotes the proliferation of cervical cancer cell
doi:
Figure Lengend Snippet: CCL17 promotes proliferation of HeLa and SiHa cells. HeLa (A) and SiHa (B) cells were incubated with rhCCL17 (0.1, 1, 10 or 100 ng/ml) or α-CCL17 (0.03, 0.3 or 3 ug/ml) for 24 h (left) or 48 h (right), then cell proliferation in HeLa and SiHa cells was detected by BrdU proliferation assay. In addition, HeLa (C) and SiHa (D) cells with different concentration of rhCCL17 (10 or 20 ng/ml) for 48, and the level of apoptosis in Hela and SiHa cells was analyzed by apoptosis assay. rhCCL17: recombinant human CCL17 protein; α-CCL17: anti-human CCL17 neutralizing antibody. The data are expressed as the mean ± SD. *P<0.05, **P<0.01 and ***P<0.01 (one-way ANOVA). NS: no statistically difference.
Article Snippet: And the secretion level of CCL17 in the culture supernatant was analyzed by
Techniques: Incubation, Proliferation Assay, Concentration Assay, Apoptosis Assay, Recombinant
Journal: American Journal of Cancer Research
Article Title: Chemokine CCL17 induced by hypoxia promotes the proliferation of cervical cancer cell
doi:
Figure Lengend Snippet: Hypoxia stimulates proliferation of HeLa and SiHa cells by CCL17/CCR4 interaction. (A) We cultured HeLa and SiHa cells under normal or hypoxic conditions for 12 h. Next, the proliferation ability of these cells was evaluated by BrdU proliferation assay. In addition, HeLa (B) and SiHa (C) cells were cultured under normoxic conditions, hypoxic conditions or hypoxic conditions plus α-CCL17 (0.3 ug/ml) for 8 h, and then cultured under normoxic conditions for another 48 h. And BrdU proliferation assay was performed to evaluate the proliferation of these cells. The data are expressed as the mean ± SD. *P<0.05, **P<0.01 and ***P<0.01 (Student’s t-test or one-way ANOVA). NS: no statistically difference.
Article Snippet: And the secretion level of CCL17 in the culture supernatant was analyzed by
Techniques: Cell Culture, Proliferation Assay
Journal: American Journal of Cancer Research
Article Title: Chemokine CCL17 induced by hypoxia promotes the proliferation of cervical cancer cell
doi:
Figure Lengend Snippet: The stimulatory effect of CCL17 on proliferation of HeLa and SiHa cells was dependent on JNK and STAT5 signaling pathway. HeLa (A) and SiHa (B) cells were stimulated with WP1066 (STAT3 inhibitor, 10 uM), N’-((4-Oxo-4H-chromen-3-yl) methylene) nicotinohydrazide (STAT5 inhibitor, 10 uM), LY294002 (AKT signal pathway, 10 uM) SP600125 (inhibitor for JNK signal, 10 uM), SB203580 (inhibitor for p38/MAPK signal, 10 uM), U0126 (inhibitor for ERK1/2 signal, 10 uM), BAY (NF-κB inhibitor, 10 uM), or pyrrolidine dithiocarbamate (PDTC, an antioxidant and an inhibitor of NF-κB, 10 uM) for 6 h, and then treated with rhCCL17 (10 ng/ml) for 48 h, with vehicle as the control. Subsequently, cells were collected and analyzed by BrdU proliferation assay. In addition, HeLa (C) and SiHa (D) cells were stimulated with STAT5 inhibitor (10 uM), inhibitor for JNK signal (10 uM) for 6 h, and then treated with or without rhCCL17 (10 ng/ml) for 48 h. BrdU proliferation assay was used to evaluate the proliferation of these cells. JNKi: treatment with inhibitor for JNK signal pathway; STAT5i: treatment with inhibitor for STAT5 signal pathway. The data are expressed as the mean ± SD. *P<0.05, **P<0.01 and ***P<0.001 (one-way ANOVA). ##P<0.01 and ###P<0.001 vs. the vehicle control (one-way ANOVA). NS: no statistically difference.
Article Snippet: And the secretion level of CCL17 in the culture supernatant was analyzed by
Techniques: Control, Proliferation Assay
Journal: American Journal of Cancer Research
Article Title: Chemokine CCL17 induced by hypoxia promotes the proliferation of cervical cancer cell
doi:
Figure Lengend Snippet: The role of CCL17/CCR4 interaction in the progression of cervical cancer. Accompanied by rapid growth of cervical cancer, hypoxia stimulates the expression of CCR4 on cervical cancer cells. The consequent things should be the higher reactivity of cervical cancer cells against CCL17. These changes in local cancer lesions may directly promote the proliferation and growth of cervical cancer cells through JNK and STAT5 signaling pathways and further stimulate the development of cervical cancer cells.
Article Snippet: And the secretion level of CCL17 in the culture supernatant was analyzed by
Techniques: Expressing, Protein-Protein interactions