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trifluoperazine  (MedChemExpress)


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    Structured Review

    MedChemExpress trifluoperazine
    Trifluoperazine, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trifluoperazine/product/MedChemExpress
    Average 93 stars, based on 6 article reviews
    trifluoperazine - by Bioz Stars, 2026-02
    93/100 stars

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    MedChemExpress trifluoperazine
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    MedChemExpress combination with trifluoperazine
    miR-27b-3p inhibited the process of angiogenesis of HUVECs. The experimental groups were as follows: i) HUVECs were transfected with C miRNA; ii) HUVECs transfected with C were stimulated by the serum of patients with hypertension; iii) HUVEC cells were transfected with miR-27b-3p I, followed by stimulation with the serum of patients with hypertension; iv) HUVECs were transfected with miR-27b-3p I, followed by stimulation with the serum of patients with hypertension and TFP; v) HUVECs transfected with miR-27b-3p M; vi) HUVECs transfected with C miRNA and treated with TFP (A) HUVECs viability was determined by CCK-8. (B) Cell migration was detected by Transwell assay. (C) Endothelial cell tube formation was determined on a layer of growth factor-reduced Matrigel. (D) The expressions of VEGF, MMP-9 and MMP-2 were detected by western blot analysis. **P<0.01 vs. C, ## P<0.01 vs. Serum+C, ^^ P<0.01 vs. Serum+miR-27b-3p I. C, control; CCK-8, Cell Counting Kit-8; I, inhibitor; M, mimic; TFP, <t>trifluoperazine;</t> MMP, matrix metalloprotenase; VEGF, vascular endothelial growth factor; HUVECs, human umbilical vein endothelial cells.
    Combination With Trifluoperazine, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    miR-27b-3p inhibited the process of angiogenesis of HUVECs. The experimental groups were as follows: i) HUVECs were transfected with C miRNA; ii) HUVECs transfected with C were stimulated by the serum of patients with hypertension; iii) HUVEC cells were transfected with miR-27b-3p I, followed by stimulation with the serum of patients with hypertension; iv) HUVECs were transfected with miR-27b-3p I, followed by stimulation with the serum of patients with hypertension and TFP; v) HUVECs transfected with miR-27b-3p M; vi) HUVECs transfected with C miRNA and treated with TFP (A) HUVECs viability was determined by CCK-8. (B) Cell migration was detected by Transwell assay. (C) Endothelial cell tube formation was determined on a layer of growth factor-reduced Matrigel. (D) The expressions of VEGF, MMP-9 and MMP-2 were detected by western blot analysis. **P<0.01 vs. C, ## P<0.01 vs. Serum+C, ^^ P<0.01 vs. Serum+miR-27b-3p I. C, control; CCK-8, Cell Counting Kit-8; I, inhibitor; M, mimic; TFP, trifluoperazine; MMP, matrix metalloprotenase; VEGF, vascular endothelial growth factor; HUVECs, human umbilical vein endothelial cells.

    Journal: Molecular Medicine Reports

    Article Title: Serum from patients with hypertension promotes endothelial dysfunction to induce trophoblast invasion through the miR-27b-3p/ATPase plasma membrane Ca 2+ transporting 1 axis

    doi: 10.3892/mmr.2021.11958

    Figure Lengend Snippet: miR-27b-3p inhibited the process of angiogenesis of HUVECs. The experimental groups were as follows: i) HUVECs were transfected with C miRNA; ii) HUVECs transfected with C were stimulated by the serum of patients with hypertension; iii) HUVEC cells were transfected with miR-27b-3p I, followed by stimulation with the serum of patients with hypertension; iv) HUVECs were transfected with miR-27b-3p I, followed by stimulation with the serum of patients with hypertension and TFP; v) HUVECs transfected with miR-27b-3p M; vi) HUVECs transfected with C miRNA and treated with TFP (A) HUVECs viability was determined by CCK-8. (B) Cell migration was detected by Transwell assay. (C) Endothelial cell tube formation was determined on a layer of growth factor-reduced Matrigel. (D) The expressions of VEGF, MMP-9 and MMP-2 were detected by western blot analysis. **P<0.01 vs. C, ## P<0.01 vs. Serum+C, ^^ P<0.01 vs. Serum+miR-27b-3p I. C, control; CCK-8, Cell Counting Kit-8; I, inhibitor; M, mimic; TFP, trifluoperazine; MMP, matrix metalloprotenase; VEGF, vascular endothelial growth factor; HUVECs, human umbilical vein endothelial cells.

    Article Snippet: The HUVECs (5×10 3 cells/ml) were inoculated into a 96-well plate. miRNA control, miR-27b-3p inhibitor or miR-27b-3p mimics was transfected into the cells, followed by stimulation with 10% serum from patients with hypertension or in combination with Trifluoperazine (TFP; MedChemExpress), which is an inhibitor of ATP2B1 ( ).

    Techniques: Transfection, CCK-8 Assay, Migration, Transwell Assay, Western Blot, Control, Cell Counting

    miR-27b-3p inhibited endothelial cell tube formation and trophoblast invasion by suppressing the expression of ATP2B1. The HUVEC experimental groups were as follows: Transfected with i) C miRNA; ii) C miRNA and stimulated by serum from patients with hypertension; iii) miR-27b-3p I, and stimulated with serum from patients with hypertension; iv) miR-27b-3p I, followed by stimulation with serum from patients with hypertension and TFP; v) miR-27b-3p M and vi) C miRNA and treated with TFP. (A) HUVECs were co-cultured with trophoblastic HTR-8/SVneo cells in Transwell plates for 5 h. HTR-8/SVneo cells invasion was detected and analyzed using ImageJ software. (B) After HTR-8/SVneo cells were isolated, the expression levels of VEGF, MMP-9 and MMP-2 were detected using western blotting. **P< 0.01 vs. C, ## P<0.01 vs. Serum+C, ^^ P<0.01 vs. Serum+miR-27b-3p I. miR, microRNA; ATP2B1, ATPase plasma membrane Ca 2+ transporting 1; TFP, trifluoperazine; C, control; I, inhibitor; M, mimic; MMP, matrix metalloproteinase; VEGF, vascular endothelial growth factor; HUVECs, human umbilical vein endothelial cells.

    Journal: Molecular Medicine Reports

    Article Title: Serum from patients with hypertension promotes endothelial dysfunction to induce trophoblast invasion through the miR-27b-3p/ATPase plasma membrane Ca 2+ transporting 1 axis

    doi: 10.3892/mmr.2021.11958

    Figure Lengend Snippet: miR-27b-3p inhibited endothelial cell tube formation and trophoblast invasion by suppressing the expression of ATP2B1. The HUVEC experimental groups were as follows: Transfected with i) C miRNA; ii) C miRNA and stimulated by serum from patients with hypertension; iii) miR-27b-3p I, and stimulated with serum from patients with hypertension; iv) miR-27b-3p I, followed by stimulation with serum from patients with hypertension and TFP; v) miR-27b-3p M and vi) C miRNA and treated with TFP. (A) HUVECs were co-cultured with trophoblastic HTR-8/SVneo cells in Transwell plates for 5 h. HTR-8/SVneo cells invasion was detected and analyzed using ImageJ software. (B) After HTR-8/SVneo cells were isolated, the expression levels of VEGF, MMP-9 and MMP-2 were detected using western blotting. **P< 0.01 vs. C, ## P<0.01 vs. Serum+C, ^^ P<0.01 vs. Serum+miR-27b-3p I. miR, microRNA; ATP2B1, ATPase plasma membrane Ca 2+ transporting 1; TFP, trifluoperazine; C, control; I, inhibitor; M, mimic; MMP, matrix metalloproteinase; VEGF, vascular endothelial growth factor; HUVECs, human umbilical vein endothelial cells.

    Article Snippet: The HUVECs (5×10 3 cells/ml) were inoculated into a 96-well plate. miRNA control, miR-27b-3p inhibitor or miR-27b-3p mimics was transfected into the cells, followed by stimulation with 10% serum from patients with hypertension or in combination with Trifluoperazine (TFP; MedChemExpress), which is an inhibitor of ATP2B1 ( ).

    Techniques: Expressing, Transfection, Cell Culture, Software, Isolation, Western Blot, Clinical Proteomics, Membrane, Control