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jak2 inhibitor ag490  (MedChemExpress)


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    MedChemExpress jak2 inhibitor ag490
    Vaccarin prevents the activation of <t>JAK2/STAT3,</t> which is mediated by NOX4. (A–C) Inhibitory effect of vaccarin on JAK2/STAT3 signaling in I/R mice ( n = 6). Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. (D, E) NOX4‐overexpressing H9c2 cells were constructed through transfection with pcDNA/NOX4. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Dunnett's post hoc test. (F–H) H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or <t>AG490</t> (10 μM) for 30 min, followed by H/R induction. Western blotting was conducted to determine the expression of p‐JAK2, JAK2, p‐STAT3, and STAT3. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Jak2 Inhibitor Ag490, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 217 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/jak2+inhibitor+ag490/AG490/pmc13399906-55-5-13
    Average 97 stars, based on 217 article reviews
    jak2 inhibitor ag490 - by Bioz Stars, 2026-09
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    1) Product Images from "Vaccarin Improves Myocardial Ischemia–Reperfusion Injury by Attenuating Oxidative Stress and Ferroptosis Through Reducing NOX4 ‐Modulated JAK2 / STAT3 Pathway Activation"

    Article Title: Vaccarin Improves Myocardial Ischemia–Reperfusion Injury by Attenuating Oxidative Stress and Ferroptosis Through Reducing NOX4 ‐Modulated JAK2 / STAT3 Pathway Activation

    Journal: The Kaohsiung Journal of Medical Sciences

    doi: 10.1002/kjm2.70226

    Vaccarin prevents the activation of JAK2/STAT3, which is mediated by NOX4. (A–C) Inhibitory effect of vaccarin on JAK2/STAT3 signaling in I/R mice ( n = 6). Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. (D, E) NOX4‐overexpressing H9c2 cells were constructed through transfection with pcDNA/NOX4. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Dunnett's post hoc test. (F–H) H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. Western blotting was conducted to determine the expression of p‐JAK2, JAK2, p‐STAT3, and STAT3. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Figure Legend Snippet: Vaccarin prevents the activation of JAK2/STAT3, which is mediated by NOX4. (A–C) Inhibitory effect of vaccarin on JAK2/STAT3 signaling in I/R mice ( n = 6). Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. (D, E) NOX4‐overexpressing H9c2 cells were constructed through transfection with pcDNA/NOX4. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Dunnett's post hoc test. (F–H) H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. Western blotting was conducted to determine the expression of p‐JAK2, JAK2, p‐STAT3, and STAT3. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Techniques Used: Activation Assay, Construct, Transfection, Plasmid Preparation, Western Blot, Expressing

    The inhibitory effects of vaccarin on H/R‐induced oxidative stress and ferroptosis in cardiomyocytes are mediated by the NOX4/JAK2/STAT3 signaling pathway. H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. (A–D) ROS and MDA production and SOD activity were determined. The experiment was repeated three times in triplicate. (E–G) The levels of Fe 2+ , GSSG, and GSH were determined. The experiment was repeated three times in triplicate. (H–J) The expression levels of SLC7A11 and GPX4 were determined. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Figure Legend Snippet: The inhibitory effects of vaccarin on H/R‐induced oxidative stress and ferroptosis in cardiomyocytes are mediated by the NOX4/JAK2/STAT3 signaling pathway. H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. (A–D) ROS and MDA production and SOD activity were determined. The experiment was repeated three times in triplicate. (E–G) The levels of Fe 2+ , GSSG, and GSH were determined. The experiment was repeated three times in triplicate. (H–J) The expression levels of SLC7A11 and GPX4 were determined. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Techniques Used: Transfection, Plasmid Preparation, Activity Assay, Expressing

    Mechanisms underlying the cardioprotective role of vaccarin in MI/R injury. Vaccarin suppressed the myocardial I/R‐induced NOX4 expression, thus inactivating the JAK2/STAT3 signaling. The suppression of NOX4‐mediated JAK2/STAT3 signaling contributed to the antioxidative and antiferroptotic effects of vaccarin in MI/R injury.
    Figure Legend Snippet: Mechanisms underlying the cardioprotective role of vaccarin in MI/R injury. Vaccarin suppressed the myocardial I/R‐induced NOX4 expression, thus inactivating the JAK2/STAT3 signaling. The suppression of NOX4‐mediated JAK2/STAT3 signaling contributed to the antioxidative and antiferroptotic effects of vaccarin in MI/R injury.

    Techniques Used: Expressing



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    Vaccarin prevents the activation of JAK2/STAT3, which is mediated by NOX4. (A–C) Inhibitory effect of vaccarin on JAK2/STAT3 signaling in I/R mice ( n = 6). Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. (D, E) NOX4‐overexpressing H9c2 cells were constructed through transfection with pcDNA/NOX4. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Dunnett's post hoc test. (F–H) H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. Western blotting was conducted to determine the expression of p‐JAK2, JAK2, p‐STAT3, and STAT3. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: The Kaohsiung Journal of Medical Sciences

    Article Title: Vaccarin Improves Myocardial Ischemia–Reperfusion Injury by Attenuating Oxidative Stress and Ferroptosis Through Reducing NOX4 ‐Modulated JAK2 / STAT3 Pathway Activation

    doi: 10.1002/kjm2.70226

    Figure Lengend Snippet: Vaccarin prevents the activation of JAK2/STAT3, which is mediated by NOX4. (A–C) Inhibitory effect of vaccarin on JAK2/STAT3 signaling in I/R mice ( n = 6). Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. (D, E) NOX4‐overexpressing H9c2 cells were constructed through transfection with pcDNA/NOX4. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Dunnett's post hoc test. (F–H) H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. Western blotting was conducted to determine the expression of p‐JAK2, JAK2, p‐STAT3, and STAT3. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: To inhibit the JAK2/STAT3 pathway, JAK2 inhibitor AG490 (10 μM; HY‐12000, purity 99.86%, MedChemExpress) was used.

    Techniques: Activation Assay, Construct, Transfection, Plasmid Preparation, Western Blot, Expressing

    The inhibitory effects of vaccarin on H/R‐induced oxidative stress and ferroptosis in cardiomyocytes are mediated by the NOX4/JAK2/STAT3 signaling pathway. H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. (A–D) ROS and MDA production and SOD activity were determined. The experiment was repeated three times in triplicate. (E–G) The levels of Fe 2+ , GSSG, and GSH were determined. The experiment was repeated three times in triplicate. (H–J) The expression levels of SLC7A11 and GPX4 were determined. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: The Kaohsiung Journal of Medical Sciences

    Article Title: Vaccarin Improves Myocardial Ischemia–Reperfusion Injury by Attenuating Oxidative Stress and Ferroptosis Through Reducing NOX4 ‐Modulated JAK2 / STAT3 Pathway Activation

    doi: 10.1002/kjm2.70226

    Figure Lengend Snippet: The inhibitory effects of vaccarin on H/R‐induced oxidative stress and ferroptosis in cardiomyocytes are mediated by the NOX4/JAK2/STAT3 signaling pathway. H9c2 cells were transfected with an empty pcDNA3.1 plasmid (vector) or pcDNA/NOX4. After 24 h of transfection, the cells were pretreated with vaccarin (10 μM) and/or AG490 (10 μM) for 30 min, followed by H/R induction. (A–D) ROS and MDA production and SOD activity were determined. The experiment was repeated three times in triplicate. (E–G) The levels of Fe 2+ , GSSG, and GSH were determined. The experiment was repeated three times in triplicate. (H–J) The expression levels of SLC7A11 and GPX4 were determined. The experiment was repeated three times. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's post hoc test. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: To inhibit the JAK2/STAT3 pathway, JAK2 inhibitor AG490 (10 μM; HY‐12000, purity 99.86%, MedChemExpress) was used.

    Techniques: Transfection, Plasmid Preparation, Activity Assay, Expressing

    Mechanisms underlying the cardioprotective role of vaccarin in MI/R injury. Vaccarin suppressed the myocardial I/R‐induced NOX4 expression, thus inactivating the JAK2/STAT3 signaling. The suppression of NOX4‐mediated JAK2/STAT3 signaling contributed to the antioxidative and antiferroptotic effects of vaccarin in MI/R injury.

    Journal: The Kaohsiung Journal of Medical Sciences

    Article Title: Vaccarin Improves Myocardial Ischemia–Reperfusion Injury by Attenuating Oxidative Stress and Ferroptosis Through Reducing NOX4 ‐Modulated JAK2 / STAT3 Pathway Activation

    doi: 10.1002/kjm2.70226

    Figure Lengend Snippet: Mechanisms underlying the cardioprotective role of vaccarin in MI/R injury. Vaccarin suppressed the myocardial I/R‐induced NOX4 expression, thus inactivating the JAK2/STAT3 signaling. The suppression of NOX4‐mediated JAK2/STAT3 signaling contributed to the antioxidative and antiferroptotic effects of vaccarin in MI/R injury.

    Article Snippet: To inhibit the JAK2/STAT3 pathway, JAK2 inhibitor AG490 (10 μM; HY‐12000, purity 99.86%, MedChemExpress) was used.

    Techniques: Expressing