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rat brain endothelial cell growth medium  (Cell Applications Inc)


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    Cell Applications Inc rat brain endothelial cell growth medium
    AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular <t>endothelial</t> cell. OPC: oligodendrocyte precursor cell.
    Rat Brain Endothelial Cell Growth Medium, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 93/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rat brain endothelial cell growth medium/product/Cell Applications Inc
    Average 93 stars, based on 23 article reviews
    rat brain endothelial cell growth medium - by Bioz Stars, 2026-02
    93/100 stars

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    1) Product Images from "Aldo-Keto Reductase 1C15 Characterization and Protection in Ischemic Brain Injury"

    Article Title: Aldo-Keto Reductase 1C15 Characterization and Protection in Ischemic Brain Injury

    Journal: Antioxidants

    doi: 10.3390/antiox12040909

    AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular endothelial cell. OPC: oligodendrocyte precursor cell.
    Figure Legend Snippet: AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular endothelial cell. OPC: oligodendrocyte precursor cell.

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Plasmid Preparation, Comparison, Cell Culture

    AKR1C15 protected BMVECs against OGD-induced cell death and BBB leakage. Primary rat BMVECs were subjected to 12 h OGD followed by reoxygenation in the presence or absence of 10 µg/mL TAT-AKR1C15. Cell viability and death were evaluated by ( A ) LDH assay and ( B ) MTT assay at 8 h after reoxygenation. In vitro BBB model was applied, and ( C ) permeability was evaluated at 6 h after reoxygenation. Data are mean ± SD. n = 4 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *** p < 0001 vs. Ctrl. ##, ### p < 0.01, 0.001 vs. OGD. ns: not significant. BMVEC: brain microvascular endothelial cells. OGD: oxygen–glucose deprivation. LDH: lactate dehydrogenase. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. BBB: blood–brain barrier.
    Figure Legend Snippet: AKR1C15 protected BMVECs against OGD-induced cell death and BBB leakage. Primary rat BMVECs were subjected to 12 h OGD followed by reoxygenation in the presence or absence of 10 µg/mL TAT-AKR1C15. Cell viability and death were evaluated by ( A ) LDH assay and ( B ) MTT assay at 8 h after reoxygenation. In vitro BBB model was applied, and ( C ) permeability was evaluated at 6 h after reoxygenation. Data are mean ± SD. n = 4 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *** p < 0001 vs. Ctrl. ##, ### p < 0.01, 0.001 vs. OGD. ns: not significant. BMVEC: brain microvascular endothelial cells. OGD: oxygen–glucose deprivation. LDH: lactate dehydrogenase. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. BBB: blood–brain barrier.

    Techniques Used: Lactate Dehydrogenase Assay, MTT Assay, In Vitro, Permeability, Comparison



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    AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular <t>endothelial</t> cell. OPC: oligodendrocyte precursor cell.
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    AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular <t>endothelial</t> cell. OPC: oligodendrocyte precursor cell.
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    Image Search Results


    AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular endothelial cell. OPC: oligodendrocyte precursor cell.

    Journal: Antioxidants

    Article Title: Aldo-Keto Reductase 1C15 Characterization and Protection in Ischemic Brain Injury

    doi: 10.3390/antiox12040909

    Figure Lengend Snippet: AKR1C15 expression in rat primary CNS cell cultures before and after OGD. AKR1C15 mRNA in primary rat CNS cell cultures was determined by real-time PCR. ( A ) Baseline AKR1C15 expression levels compared to TAT-AKR1C15 plasmid (Biomatik). Data are mean ± SD. n = 6–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, *** p < 0.05, 0.001 vs. Neuron. ns: not significant. Cell cultures were then subjected to OGD/reoxygenation, and AKR1C15 mRNA expressions were detected at 2, 8, and 24 h after reoxygenation in cultured ( B ) neurons (1 h OGD), ( C ) OPCs (90 min OGD), ( D ) astrocytes (4 h OGD), ( E ) BMVECs (12 h OGD), and ( F ) microglia (90 min OGD). Data are mean ± SD. n = 4–9 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *, **, *** p < 0.05, 0.01, 0.001 vs. Ctrl. OGD: oxygen–glucose deprivation. BMVEC: brain microvascular endothelial cell. OPC: oligodendrocyte precursor cell.

    Article Snippet: Primary rat brain microvascular endothelial cells (BMVECs) were purchased from Cell Applications (San Diego, CA, USA) and were maintained in rat brain endothelial cell growth medium consisting of basal medium and appropriate growth factors (Cell Applications, San Diego, CA, USA).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Plasmid Preparation, Comparison, Cell Culture

    AKR1C15 protected BMVECs against OGD-induced cell death and BBB leakage. Primary rat BMVECs were subjected to 12 h OGD followed by reoxygenation in the presence or absence of 10 µg/mL TAT-AKR1C15. Cell viability and death were evaluated by ( A ) LDH assay and ( B ) MTT assay at 8 h after reoxygenation. In vitro BBB model was applied, and ( C ) permeability was evaluated at 6 h after reoxygenation. Data are mean ± SD. n = 4 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *** p < 0001 vs. Ctrl. ##, ### p < 0.01, 0.001 vs. OGD. ns: not significant. BMVEC: brain microvascular endothelial cells. OGD: oxygen–glucose deprivation. LDH: lactate dehydrogenase. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. BBB: blood–brain barrier.

    Journal: Antioxidants

    Article Title: Aldo-Keto Reductase 1C15 Characterization and Protection in Ischemic Brain Injury

    doi: 10.3390/antiox12040909

    Figure Lengend Snippet: AKR1C15 protected BMVECs against OGD-induced cell death and BBB leakage. Primary rat BMVECs were subjected to 12 h OGD followed by reoxygenation in the presence or absence of 10 µg/mL TAT-AKR1C15. Cell viability and death were evaluated by ( A ) LDH assay and ( B ) MTT assay at 8 h after reoxygenation. In vitro BBB model was applied, and ( C ) permeability was evaluated at 6 h after reoxygenation. Data are mean ± SD. n = 4 independent experiments. One-way ANOVA followed by Tukey’s multiple comparison. *** p < 0001 vs. Ctrl. ##, ### p < 0.01, 0.001 vs. OGD. ns: not significant. BMVEC: brain microvascular endothelial cells. OGD: oxygen–glucose deprivation. LDH: lactate dehydrogenase. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. BBB: blood–brain barrier.

    Article Snippet: Primary rat brain microvascular endothelial cells (BMVECs) were purchased from Cell Applications (San Diego, CA, USA) and were maintained in rat brain endothelial cell growth medium consisting of basal medium and appropriate growth factors (Cell Applications, San Diego, CA, USA).

    Techniques: Lactate Dehydrogenase Assay, MTT Assay, In Vitro, Permeability, Comparison