h9c2(2-1) Search Results


h9c2 crl 1446  (ATCC)
99
ATCC h9c2 crl 1446
H9c2 Crl 1446, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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h9c2 cells  (CLS Cell Lines Service GmbH)
93
CLS Cell Lines Service GmbH h9c2 cells
H9c2 Cells, supplied by CLS Cell Lines Service GmbH, 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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h9c2 cells  (Elabscience Biotechnology)
93
Elabscience Biotechnology h9c2 cells
Dipyridamole inhibits ferroptotic cell death in myocardium cells. a) Cell death measurement of <t>H9c2</t> cells treated with RSL3 (250 and 500 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 4 h. Dead cells were labeled with SYTOX Green. b–d) The relative mRNA levels of Ptgs2 (b), Bnp (c), and Myh7 (d) were quantified by qRT‐PCR in H9c2 cells. e) Immunofluorescence staining of BODIPY 581/591 C11 to detect the levels of lipid peroxidation in the H9c2 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ) and dipyridamole (10 µ m ) for 4 h. f) Dose‐dependent toxicity of RSL3‐induced cell death in AC16 cells after pre‐treatment with dipyridamole (10 µ m ) for 12 h. Cell viability was assessed 12 h post‐treatment after using CCK8. g) Cell death measurement of AC16 cells treated with RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 6 h. Dead cells were labeled with SYTOX Green. h,i) The relative mRNA levels of PTGS2 (h) and CHAC1 (i) were quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 3 h. j,k) BODIPYTM 581/591 C11 staining of lipid peroxidation in AC16 cells treated with DMSO, RSL3 (200 n m ), Lipro‐1(4 µ m ) or dipyridamole (10 µ m ) for 3 h. l) The relative mRNA level of BNP was quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (400 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 3 h. m,n) The relative mRNA level of Ptgs2 was quantified by qRT‐PCR in H9c2 cells (m) and NCM (n) pretreated with Lipro‐1 (4 µ m ) or dipyridamole (10 µ m ) for 4 h, followed by hypoxia/reoxygenation (H/R). Data and error bars are mean ± SEM, n = 3 biologically independent experiments in a–d and f‐n. All P values were calculated using a two‐tailed, unpaired Student's t ‐test.
H9c2 Cells, supplied by Elabscience Biotechnology, 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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crl-1446  (atcc)
96
atcc crl-1446
Dipyridamole inhibits ferroptotic cell death in myocardium cells. a) Cell death measurement of <t>H9c2</t> cells treated with RSL3 (250 and 500 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 4 h. Dead cells were labeled with SYTOX Green. b–d) The relative mRNA levels of Ptgs2 (b), Bnp (c), and Myh7 (d) were quantified by qRT‐PCR in H9c2 cells. e) Immunofluorescence staining of BODIPY 581/591 C11 to detect the levels of lipid peroxidation in the H9c2 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ) and dipyridamole (10 µ m ) for 4 h. f) Dose‐dependent toxicity of RSL3‐induced cell death in AC16 cells after pre‐treatment with dipyridamole (10 µ m ) for 12 h. Cell viability was assessed 12 h post‐treatment after using CCK8. g) Cell death measurement of AC16 cells treated with RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 6 h. Dead cells were labeled with SYTOX Green. h,i) The relative mRNA levels of PTGS2 (h) and CHAC1 (i) were quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 3 h. j,k) BODIPYTM 581/591 C11 staining of lipid peroxidation in AC16 cells treated with DMSO, RSL3 (200 n m ), Lipro‐1(4 µ m ) or dipyridamole (10 µ m ) for 3 h. l) The relative mRNA level of BNP was quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (400 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 3 h. m,n) The relative mRNA level of Ptgs2 was quantified by qRT‐PCR in H9c2 cells (m) and NCM (n) pretreated with Lipro‐1 (4 µ m ) or dipyridamole (10 µ m ) for 4 h, followed by hypoxia/reoxygenation (H/R). Data and error bars are mean ± SEM, n = 3 biologically independent experiments in a–d and f‐n. All P values were calculated using a two‐tailed, unpaired Student's t ‐test.
Crl 1446, supplied by atcc, 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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rat heart-derived embryonic myoblast h9c2 cells  (DS Pharma Biomedical)
90
DS Pharma Biomedical rat heart-derived embryonic myoblast h9c2 cells
Dipyridamole inhibits ferroptotic cell death in myocardium cells. a) Cell death measurement of <t>H9c2</t> cells treated with RSL3 (250 and 500 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 4 h. Dead cells were labeled with SYTOX Green. b–d) The relative mRNA levels of Ptgs2 (b), Bnp (c), and Myh7 (d) were quantified by qRT‐PCR in H9c2 cells. e) Immunofluorescence staining of BODIPY 581/591 C11 to detect the levels of lipid peroxidation in the H9c2 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ) and dipyridamole (10 µ m ) for 4 h. f) Dose‐dependent toxicity of RSL3‐induced cell death in AC16 cells after pre‐treatment with dipyridamole (10 µ m ) for 12 h. Cell viability was assessed 12 h post‐treatment after using CCK8. g) Cell death measurement of AC16 cells treated with RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 6 h. Dead cells were labeled with SYTOX Green. h,i) The relative mRNA levels of PTGS2 (h) and CHAC1 (i) were quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 3 h. j,k) BODIPYTM 581/591 C11 staining of lipid peroxidation in AC16 cells treated with DMSO, RSL3 (200 n m ), Lipro‐1(4 µ m ) or dipyridamole (10 µ m ) for 3 h. l) The relative mRNA level of BNP was quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (400 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 3 h. m,n) The relative mRNA level of Ptgs2 was quantified by qRT‐PCR in H9c2 cells (m) and NCM (n) pretreated with Lipro‐1 (4 µ m ) or dipyridamole (10 µ m ) for 4 h, followed by hypoxia/reoxygenation (H/R). Data and error bars are mean ± SEM, n = 3 biologically independent experiments in a–d and f‐n. All P values were calculated using a two‐tailed, unpaired Student's t ‐test.
Rat Heart Derived Embryonic Myoblast H9c2 Cells, supplied by DS Pharma Biomedical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rat heart-derived embryonic myoblast h9c2 cells - by Bioz Stars, 2026-05
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h9c2(2–1) cell avalanchetm transfection reagent  (EZ Biosystems)
90
EZ Biosystems h9c2(2–1) cell avalanchetm transfection reagent
Dipyridamole inhibits ferroptotic cell death in myocardium cells. a) Cell death measurement of <t>H9c2</t> cells treated with RSL3 (250 and 500 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 4 h. Dead cells were labeled with SYTOX Green. b–d) The relative mRNA levels of Ptgs2 (b), Bnp (c), and Myh7 (d) were quantified by qRT‐PCR in H9c2 cells. e) Immunofluorescence staining of BODIPY 581/591 C11 to detect the levels of lipid peroxidation in the H9c2 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ) and dipyridamole (10 µ m ) for 4 h. f) Dose‐dependent toxicity of RSL3‐induced cell death in AC16 cells after pre‐treatment with dipyridamole (10 µ m ) for 12 h. Cell viability was assessed 12 h post‐treatment after using CCK8. g) Cell death measurement of AC16 cells treated with RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 6 h. Dead cells were labeled with SYTOX Green. h,i) The relative mRNA levels of PTGS2 (h) and CHAC1 (i) were quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 3 h. j,k) BODIPYTM 581/591 C11 staining of lipid peroxidation in AC16 cells treated with DMSO, RSL3 (200 n m ), Lipro‐1(4 µ m ) or dipyridamole (10 µ m ) for 3 h. l) The relative mRNA level of BNP was quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (400 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 3 h. m,n) The relative mRNA level of Ptgs2 was quantified by qRT‐PCR in H9c2 cells (m) and NCM (n) pretreated with Lipro‐1 (4 µ m ) or dipyridamole (10 µ m ) for 4 h, followed by hypoxia/reoxygenation (H/R). Data and error bars are mean ± SEM, n = 3 biologically independent experiments in a–d and f‐n. All P values were calculated using a two‐tailed, unpaired Student's t ‐test.
H9c2(2–1) Cell Avalanchetm Transfection Reagent, supplied by EZ Biosystems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/h9c2(2–1) cell avalanchetm transfection reagent/product/EZ Biosystems
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h9c2(2-1) cell lines complete growth medium  (Innovative Research Inc)
N/A
H9c2(2-1) Cell Lines Complete Growth Medium is a cell lines complete growth medium from Innovative Research, supplied as a ready-to-use liquid. More Details: Formulation: DMEM + 10% FBS + 1% P/S Bacterial detection: Negative Fungal
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h9c2 2 1 cell line  (Elabscience)
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Dipyridamole inhibits ferroptotic cell death in myocardium cells. a) Cell death measurement of H9c2 cells treated with RSL3 (250 and 500 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 4 h. Dead cells were labeled with SYTOX Green. b–d) The relative mRNA levels of Ptgs2 (b), Bnp (c), and Myh7 (d) were quantified by qRT‐PCR in H9c2 cells. e) Immunofluorescence staining of BODIPY 581/591 C11 to detect the levels of lipid peroxidation in the H9c2 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ) and dipyridamole (10 µ m ) for 4 h. f) Dose‐dependent toxicity of RSL3‐induced cell death in AC16 cells after pre‐treatment with dipyridamole (10 µ m ) for 12 h. Cell viability was assessed 12 h post‐treatment after using CCK8. g) Cell death measurement of AC16 cells treated with RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 6 h. Dead cells were labeled with SYTOX Green. h,i) The relative mRNA levels of PTGS2 (h) and CHAC1 (i) were quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 3 h. j,k) BODIPYTM 581/591 C11 staining of lipid peroxidation in AC16 cells treated with DMSO, RSL3 (200 n m ), Lipro‐1(4 µ m ) or dipyridamole (10 µ m ) for 3 h. l) The relative mRNA level of BNP was quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (400 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 3 h. m,n) The relative mRNA level of Ptgs2 was quantified by qRT‐PCR in H9c2 cells (m) and NCM (n) pretreated with Lipro‐1 (4 µ m ) or dipyridamole (10 µ m ) for 4 h, followed by hypoxia/reoxygenation (H/R). Data and error bars are mean ± SEM, n = 3 biologically independent experiments in a–d and f‐n. All P values were calculated using a two‐tailed, unpaired Student's t ‐test.

Journal: Advanced Science

Article Title: Dipyridamole Acts as Clinical Ferroptosis Inhibitor to Prevent from Tissue Injury

doi: 10.1002/advs.202500566

Figure Lengend Snippet: Dipyridamole inhibits ferroptotic cell death in myocardium cells. a) Cell death measurement of H9c2 cells treated with RSL3 (250 and 500 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 4 h. Dead cells were labeled with SYTOX Green. b–d) The relative mRNA levels of Ptgs2 (b), Bnp (c), and Myh7 (d) were quantified by qRT‐PCR in H9c2 cells. e) Immunofluorescence staining of BODIPY 581/591 C11 to detect the levels of lipid peroxidation in the H9c2 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ) and dipyridamole (10 µ m ) for 4 h. f) Dose‐dependent toxicity of RSL3‐induced cell death in AC16 cells after pre‐treatment with dipyridamole (10 µ m ) for 12 h. Cell viability was assessed 12 h post‐treatment after using CCK8. g) Cell death measurement of AC16 cells treated with RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 6 h. Dead cells were labeled with SYTOX Green. h,i) The relative mRNA levels of PTGS2 (h) and CHAC1 (i) were quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (200 n m ), dipyridamole (10 µ m ), and Fer‐1 (4 µ m ) for 3 h. j,k) BODIPYTM 581/591 C11 staining of lipid peroxidation in AC16 cells treated with DMSO, RSL3 (200 n m ), Lipro‐1(4 µ m ) or dipyridamole (10 µ m ) for 3 h. l) The relative mRNA level of BNP was quantified by qRT‐PCR in AC16 cells treated with DMSO, RSL3 (400 n m ), dipyridamole (10 µ m ), or Fer‐1 (4 µ m ) for 3 h. m,n) The relative mRNA level of Ptgs2 was quantified by qRT‐PCR in H9c2 cells (m) and NCM (n) pretreated with Lipro‐1 (4 µ m ) or dipyridamole (10 µ m ) for 4 h, followed by hypoxia/reoxygenation (H/R). Data and error bars are mean ± SEM, n = 3 biologically independent experiments in a–d and f‐n. All P values were calculated using a two‐tailed, unpaired Student's t ‐test.

Article Snippet: H9c2 cells were exposed to RSL3, Fer‐1 (4 μ m ) or dipyridamole (10 μ m ) for 6 h. 1 × 10 6 cells per sample were collected and intracellular CK‐MB or BNP levels were determined using the Rat CK‐MB (Creatine Kinase MB Isoenzyme) ELISA Kit (Elabscience, E‐EL‐R1327) and Rat BNP (Brain Natriuretic Peptide) ELISA Kit (E‐EL‐R0126) according to the manufacturer's instructions.

Techniques: Labeling, Quantitative RT-PCR, Immunofluorescence, Staining, Two Tailed Test

Dipyridamole‐mediated ferroptosis depends on SLC7A11. a,b) Immunoblot assays of classical ferroptosis‐related genes in HT1080 (a) and H9c2 (b) cells with dipyridamole (20 µ m ) treatment at indicated times. c‐e) Immunoblot assays of SLC7A11 expression in HT1080 (c), OVCAR8 (d), and 786‐O (e) cells with dipyridamole (20 µ m ) treatment at indicated times. f) Immunoblot assays of SLC7A11 expression in HT1080 WT and SLC7A11 KO cells. g) Cell viability assay in HT1080 WT and SLC7A11 KO cells treated with DMSO, dipyridamole (20 µ m ), or RSL3 at the indicated concentration. h) The GSH levels in HT1080 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ), and dipyridamole (10 µ m ) for 4 h. i) Immunoblot assays of exogenous SLC7A11 expression in HT1080 SLC7A11 KO cells stably expressing with the Mock and SLC7A11‐Flag vector. j) Cell viability assay in HT1080 SLC7A11 KO cells stably expressing with the Mock and SLC7A11‐Flag vector treated with DMSO, RSL3 (5 µ m ), and dipyridamole (10 µ m ) at the indicated concentration. k) The cell death of HT1080 SLC7A11 KO cells stably expressing the Mock and SLC7A11‐Flag vector was measured. These cells were treated with DMSO, RSL3 (5 µ m ), or dipyridamole (10 µ m ) for 6 h. Dead cells were labeled with SYTOX™ Green. Data and error bars are mean ± SEM, n = 3 biologically independent experiments in g, h, j, and k. All P values were calculated using a two‐tailed, unpaired Student's t‐test.

Journal: Advanced Science

Article Title: Dipyridamole Acts as Clinical Ferroptosis Inhibitor to Prevent from Tissue Injury

doi: 10.1002/advs.202500566

Figure Lengend Snippet: Dipyridamole‐mediated ferroptosis depends on SLC7A11. a,b) Immunoblot assays of classical ferroptosis‐related genes in HT1080 (a) and H9c2 (b) cells with dipyridamole (20 µ m ) treatment at indicated times. c‐e) Immunoblot assays of SLC7A11 expression in HT1080 (c), OVCAR8 (d), and 786‐O (e) cells with dipyridamole (20 µ m ) treatment at indicated times. f) Immunoblot assays of SLC7A11 expression in HT1080 WT and SLC7A11 KO cells. g) Cell viability assay in HT1080 WT and SLC7A11 KO cells treated with DMSO, dipyridamole (20 µ m ), or RSL3 at the indicated concentration. h) The GSH levels in HT1080 cells treated with RSL3 (250 n m ), Fer‐1(4 µ m ), and dipyridamole (10 µ m ) for 4 h. i) Immunoblot assays of exogenous SLC7A11 expression in HT1080 SLC7A11 KO cells stably expressing with the Mock and SLC7A11‐Flag vector. j) Cell viability assay in HT1080 SLC7A11 KO cells stably expressing with the Mock and SLC7A11‐Flag vector treated with DMSO, RSL3 (5 µ m ), and dipyridamole (10 µ m ) at the indicated concentration. k) The cell death of HT1080 SLC7A11 KO cells stably expressing the Mock and SLC7A11‐Flag vector was measured. These cells were treated with DMSO, RSL3 (5 µ m ), or dipyridamole (10 µ m ) for 6 h. Dead cells were labeled with SYTOX™ Green. Data and error bars are mean ± SEM, n = 3 biologically independent experiments in g, h, j, and k. All P values were calculated using a two‐tailed, unpaired Student's t‐test.

Article Snippet: H9c2 cells were exposed to RSL3, Fer‐1 (4 μ m ) or dipyridamole (10 μ m ) for 6 h. 1 × 10 6 cells per sample were collected and intracellular CK‐MB or BNP levels were determined using the Rat CK‐MB (Creatine Kinase MB Isoenzyme) ELISA Kit (Elabscience, E‐EL‐R1327) and Rat BNP (Brain Natriuretic Peptide) ELISA Kit (E‐EL‐R0126) according to the manufacturer's instructions.

Techniques: Western Blot, Expressing, Viability Assay, Concentration Assay, Stable Transfection, Plasmid Preparation, Labeling, Two Tailed Test