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Image Search Results
Journal: bioRxiv
Article Title: ASK1/p38-mediated NLRP3 inflammasome signaling pathway contributed to aberrant retinal angiogenesis in diabetic retinopathy
doi: 10.1101/763102
Figure Lengend Snippet: (A) The inflammatory related cytokine IL-6, TNF-α and IL-1β mRNA expression levels were enhanced in DR group. (B) The expression of vascular marker CD31 was increased in DR group by confocal detection. Meanwhile, (C) the VEGF secretion levels in DR group was increased compared with control group. Values are expressed as the mean ± SD (n = 6, *P < 0.05, **P < 0.01 and ***P < 0.001 compared with the control).
Article Snippet: The retinal tissue from control group, HG group and HG treated with inhibitor group were added in PBS and homogenized; the homogenate was centrifuged at 12000 g at 4°C for 10 min. Then, the supernatant was tested for VEGF by
Techniques: Expressing, Marker, Control
Journal: bioRxiv
Article Title: ASK1/p38-mediated NLRP3 inflammasome signaling pathway contributed to aberrant retinal angiogenesis in diabetic retinopathy
doi: 10.1101/763102
Figure Lengend Snippet: (A) The protein expression level of NLRP3 was enhanced in DR groups; moreover, (B) blocking NLRP3, the mRNA expression of IL-6, TNF-α and IL-1β was down-regulated; meanwhile, (C) the vascular marker CD31 expression level and (D) VEGF secretion level were decreased through inhibiting NLRP3. In addition, in HRMEC cell model, (E) high glucose enhanced the protein expression of NLRP3, which was inhibited by NLPR3 inhibitor. (F) The inflammatory related cytokine IL-6, TNF-α and IL-1β was enhanced in HG-induced HRMEC cell model and was inhibited through blocking NLRP3. (G) The VEGF secretion level was enhanced, and was decreased after inhibiting NLRP3. Data are presented as the mean ± standard deviation from triplicate wells. *P < 0.05 and **P < 0.01 compared with the control. #P < 0.05 and ## P < 0.01 compared with the relative DR animal model group or HG-induced HRMEC cell group.
Article Snippet: The retinal tissue from control group, HG group and HG treated with inhibitor group were added in PBS and homogenized; the homogenate was centrifuged at 12000 g at 4°C for 10 min. Then, the supernatant was tested for VEGF by
Techniques: Expressing, Blocking Assay, Marker, Standard Deviation, Control, Animal Model
Journal: bioRxiv
Article Title: ASK1/p38-mediated NLRP3 inflammasome signaling pathway contributed to aberrant retinal angiogenesis in diabetic retinopathy
doi: 10.1101/763102
Figure Lengend Snippet: (A) The protein expression levels of AKS1 and p38 were up-regulated in DR animal group. (B)The result of HG-induced HRMEC group was similar with DR animal group. Moreover, (C) the NLPR3, IL-6, TNF-α, IL-1β and VEGF protein expression levels were inhibited by (C) NLPR3 inhibitor and (D) p38 inhibitor.
Article Snippet: The retinal tissue from control group, HG group and HG treated with inhibitor group were added in PBS and homogenized; the homogenate was centrifuged at 12000 g at 4°C for 10 min. Then, the supernatant was tested for VEGF by
Techniques: Expressing
Journal: Frontiers in Immunology
Article Title: Natural Killer-Like B Cells Secreting Interleukin-18 Induces a Proinflammatory Response in Periodontitis
doi: 10.3389/fimmu.2021.641562
Figure Lengend Snippet: IL-18 regulates the inflammatory reaction of periodontal ligament cells in vitro . Periodontal ligament cells were isolated from five healthy individuals who underwent routine premolar procedures for orthodontic reasons and were stimulated with recombinant human IL-18 for 48 h. (A) Proliferation of periodontal ligament cells was measured by Cell Counting Kit-8. (B) Cell cycle and apoptosis was assessed by flow cytometry. Expression of (C) Interferon-γ (IFN-γ), (D) granulocyte macrophage-colony stimulating factor (GM-CSF), (E) IL-2, and (F) tumor necrosis factor-α (TNF-α) was measured by ELISA. Data are expressed as mean ± standard deviation. Group differences were assessed by paired t -test.
Article Snippet: Interferon-γ (IFN-γ), granulocyte macrophage-colony stimulating factor (GM-CSF), IL-2, and tumor necrosis factor-α (TNF-α) levels in the cultured supernatants were measured by
Techniques: In Vitro, Isolation, Recombinant, Cell Counting, Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Standard Deviation