Journal: Frontiers in pharmacology

Article Title: Curcumin Derivative Cur20 Attenuated Cerebral Ischemic Injury by Antioxidant Effect and HIF-1α/VEGF/TFEB-Activated Angiogenesis.

doi: 10.3389/fphar.2021.648107

Figure Lengend Snippet: FIGURE 6 | Expression of HIF-1 a (A), VEGF (B), TFEB (C), and CD34 (D) in cerebral cortex analyzed by immunohistochemistry. *p < 0.05 vs. sham group, **p < 0.01 vs. sham group; #p < 0.05 vs. Model group, ##p < 0.01 vs. Model group.

Article Snippet: Brain slices were incubated with antibodies (BosterBioengineering, Wuhan, China) against HIF-1α, CD34, NF-κB, VEGF, TFEB (rabbit polyclonal IgGantibody; 1:100) at 4°C and reacted with avidin-biotin-peroxidase complex and DAB (Boster Bio-engineering, Wuhan, China).

Techniques: Expressing, Immunohistochemistry

Journal: Frontiers in pharmacology

Article Title: Curcumin Derivative Cur20 Attenuated Cerebral Ischemic Injury by Antioxidant Effect and HIF-1α/VEGF/TFEB-Activated Angiogenesis.

doi: 10.3389/fphar.2021.648107

Figure Lengend Snippet: FIGURE 9 | Effect of Cur20 on the HIF-1α/VEGF/TFEB pathway. A–E, The protein levels of HIF-1α, NF-κB, VEGF, and TFEB analyzed by western blot. F, The content and translocation of TFEB in nuclei observed by confocal microscopy with immunofluorescence. rBMECs were pretreated with Cur20 for 2 h then treated with OGD for 4 h. L, M, or H represents the concentration of Cur20 as 0.1, 1, 10 μM, respectively. In the immunofluorescence experiment, the concentration of Cur20 was 10 μM. The experimental data was expressed by mean ± SD, n 3.*p < 0.05 vs. control group, #p < 0.05 vs. Model group.

Article Snippet: Brain slices were incubated with antibodies (BosterBioengineering, Wuhan, China) against HIF-1α, CD34, NF-κB, VEGF, TFEB (rabbit polyclonal IgGantibody; 1:100) at 4°C and reacted with avidin-biotin-peroxidase complex and DAB (Boster Bio-engineering, Wuhan, China).

Techniques: Western Blot, Translocation Assay, Confocal Microscopy, Concentration Assay, Control

Journal: Cell death & disease

Article Title: B7-H3 promotes colorectal cancer angiogenesis through activating the NF-κB pathway to induce VEGFA expression.

doi: 10.1038/s41419-020-2252-3

Figure Lengend Snippet: Fig. 3 B7-H3 promoted the expression of VEGFA in CRC. a The expression of angiogenesis-related genes was detected by RT-qPCR in shB7-H3 HCT116 and RKO cells. b Western blot analysis of B7-H3 and VEGFA in the sh-NC and shB7-H3 CRC cell lines. β-actin served as a loading control. c Representative images of IHC for VEGFA in CRC tissues and matched normal tissues from the 125 clinical CRC patients. Scale bar, 100 μm. d VEGFA protein expression based on the staining index of CRC specimens and matched normal tissues. e VEGFA protein expression is shown for patients stratified into B7-H3 low (median value) groups. f Correlation analysis of the staining index of the protein expression levels of B7-H3 and CD31 in human CRC specimens (n = 125). The correlation coefficient (r) is shown. The data represent the means ± SEM. NS no significant difference; *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: After antigen retrieval with 10mM sodium citrate buffer (pH 6.0), the sections were incubated with goat anti-human 4IgB7-H3 antibody (R&D Systems, MN, USA, #AF1027, 1:100), mouse anti-human CD31 antibody (Abcam, Cambridge, MA, USA, #ab32457, 1:1500), or rabbit anti-human VEGFA antibody (Proteintech, Wuhan, China, #19003–1-AP, 1:500).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control, Staining

Journal: Cell death & disease

Article Title: B7-H3 promotes colorectal cancer angiogenesis through activating the NF-κB pathway to induce VEGFA expression.

doi: 10.1038/s41419-020-2252-3

Figure Lengend Snippet: Fig. 6 B7-H3 promoted angiogenesis via NF-κB/VEGFA pathway in Matrigel plugs in vivo. a, b CD31 (a) and VEGFA (b) protein expression based on their IHC staining index results in subcutaneous tumors formed by sh-NC-HCT116 and shB7-H3-HCT116 cells. N = 5. c, d CD31 (c) and VEGFA (d) protein expression based on their IHC staining index results in subcutaneous tumors formed by EV-HCT116 and B7-H3-HCT116 cells. N = 5. e, f CD31 (e) and VEGFA (f) protein expression based on their IHC staining index results in subcutaneous B7-H3-HCT116 tumors and B7-H3-HCT116 tumors treated with BAY11–7082 (6 mg/kg). g, h CD31 (g) and VEGFA (h) protein expression based on their IHC staining index results in subcutaneous B7-H3-HCT116 tumors and B7-H3-HCT116 tumors treated with bevacizumab (1 mg/kg). i, j CD31 (i) and VEGFA (j) protein expression based on their IHC staining index results in subcutaneous B7-H3-HCT116 tumors and B7-H3-HCT116 tumors co-treated with 3E8 (5 mg/kg) and BAY11–7082 (6 mg/kg) or bevacizumab (1 mg/kg). N = 5. The data represent the means ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: After antigen retrieval with 10mM sodium citrate buffer (pH 6.0), the sections were incubated with goat anti-human 4IgB7-H3 antibody (R&D Systems, MN, USA, #AF1027, 1:100), mouse anti-human CD31 antibody (Abcam, Cambridge, MA, USA, #ab32457, 1:1500), or rabbit anti-human VEGFA antibody (Proteintech, Wuhan, China, #19003–1-AP, 1:500).

Techniques: In Vivo, Expressing, Immunohistochemistry