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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
Cell Counting Kit 8 Cck8 Assay, supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 <t>(CCK8).</t> (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.
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Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 (CCK8). (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.

Journal: iScience

Article Title: Active and passive targeted delivery of anti-ferroptotic therapy for post-resuscitation myocardial dysfunction

doi: 10.1016/j.isci.2025.113174

Figure Lengend Snippet: Cardiomyocyte toxicity testing and APTD@Fer-1 reduces hypoxia/reoxygenation (H/R) damage by inhibiting cardiomyocyte ferroptosis (A) H9c2 cytotoxicity of APTD loaded and unloaded ( n = 3) nanomicelles using cell-counting kit 8 (CCK8). (B) After H/R, cell viability is detected using the CCK8 kit on H9c2 cells ( n = 3) from different treatment groups. (C) LDH level in the medium of the indicated group. (D) The level of ferroptotic marker Ptgs2 mRNA in the indicated group, normalized using mRNA levels of the Gapdh gene. (E and F) Oxidation level markers SOD and MDA in the indicated group. (G) Total non-heme iron level in the indicated group (C–G, n = 6). Summary data are recorded as the mean ± standard deviation. Significance is calculated using a one-way ANOVA with Tukey’s post-hoc test, ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001, ns = no significance.

Article Snippet: H9c2 cardiomyocytes (5 × 10 3 /cell) were co-cultured with drug-loaded nanocarrier APTD@Fer-1 NPs and empty APTD NPs (at a material concentration of 0.1 mg/mL) for 12, 24, and 48 h. Cell viability was determined using the CCK8 cell proliferation assay kit (10 μL/well; MedChemExpress, Monmouth Junction, NJ, USA) by measuring the absorbance at 450 nm and calculating the cell survival rate.

Techniques: Cell Counting, Marker, Standard Deviation

Journal: iScience

Article Title: Active and passive targeted delivery of anti-ferroptotic therapy for post-resuscitation myocardial dysfunction

doi: 10.1016/j.isci.2025.113174

Figure Lengend Snippet:

Article Snippet: H9c2 cardiomyocytes (5 × 10 3 /cell) were co-cultured with drug-loaded nanocarrier APTD@Fer-1 NPs and empty APTD NPs (at a material concentration of 0.1 mg/mL) for 12, 24, and 48 h. Cell viability was determined using the CCK8 cell proliferation assay kit (10 μL/well; MedChemExpress, Monmouth Junction, NJ, USA) by measuring the absorbance at 450 nm and calculating the cell survival rate.

Techniques: Recombinant, Iron Assay, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Lactate Dehydrogenase Assay, TBARS Assay, Colorimetric Assay, Software