carbocyanines and 20-hydroxy-5-8-11-14-eicosatetraenoic-acid

carbocyanines has been researched along with 20-hydroxy-5-8-11-14-eicosatetraenoic-acid* in 1 studies

Other Studies

1 other study(ies) available for carbocyanines and 20-hydroxy-5-8-11-14-eicosatetraenoic-acid

Article	Year
20-Hydroxyeicosatetraenoic acid induces apoptosis in neonatal rat cardiomyocytes through mitochondrial-dependent pathways. Journal of cardiovascular pharmacology, 2011, Volume: 57, Issue:3 20-Hydroxyeicosatetraenoic acid (20-HETE), a [omega]-hydroxylation product of arachidonic acid catalyzed by cytochrome P450 4A, may play a role in the cardiovascular system. It is well known that cytochrome P450 [omega]-hydroxylase inhibitors markedly reduced the cardiac ischemia reperfusion injury. However, the direct effect of 20-HETE on cardiomyocytes is still poorly investigated. Here, we studied the effect of 20-HETE on cardiomyocyte apoptosis and the apoptosis-associated signaling pathways.. The cardiomyocyte apoptosis was measured by fluorescein isothiocyanate conjugated annexin V/propidium iodide double staining cytometry, indicating that the percentage of early apoptotic cells increased from 15.6% +/- 2.6% to 25.5% +/- 2.5% in control and 20-HETE-treated cells, respectively. The mitochondrial membrane potential ([DELTA][PSI]m) was measured by detecting the ratio of JC-1 green/red emission intensity. A significant decrease in the ratio was observed after treatment with 20-HETE for 24 hours in comparison with control group, suggesting the disruptive effect of 20-HETE on mitochondrial [DELTA][PSI]m. In addition, 20-HETE stimulated caspase-3 activity and Bax mRNA expression in cardiomyocytes. In contrast, the Bcl-2 mRNA levels were significantly decreased by 20-HETE treatment.. These results demonstrate that 20-HETE induces cardiomyocyte apoptosis by activation of several intrinsic apoptotic pathways. The 20-HETE-induced apoptosis could contribute to the cytochrome P450 [omega]-hydroxylase-dependent cardiac injure during cardiac ischemia-reperfusion. Topics: Amidines; Animals; Animals, Newborn; Apoptosis; Arachidonic Acid; bcl-2-Associated X Protein; Benzimidazoles; Carbocyanines; Caspase 3; Cell Survival; Cytochrome P-450 CYP4A; Cytochrome P-450 Enzyme Inhibitors; Cytochrome P-450 Enzyme System; Fluorescent Dyes; Genes, bcl-2; Hydroxyeicosatetraenoic Acids; Hydroxylation; Membrane Potential, Mitochondrial; Mitochondria; Myocytes, Cardiac; Rats; Rats, Wistar; Signal Transduction; Staining and Labeling	2011

Article

Year

20-Hydroxyeicosatetraenoic acid induces apoptosis in neonatal rat cardiomyocytes through mitochondrial-dependent pathways.

Journal of cardiovascular pharmacology, 2011, Volume: 57, Issue:3

20-Hydroxyeicosatetraenoic acid (20-HETE), a [omega]-hydroxylation product of arachidonic acid catalyzed by cytochrome P450 4A, may play a role in the cardiovascular system. It is well known that cytochrome P450 [omega]-hydroxylase inhibitors markedly reduced the cardiac ischemia reperfusion injury. However, the direct effect of 20-HETE on cardiomyocytes is still poorly investigated. Here, we studied the effect of 20-HETE on cardiomyocyte apoptosis and the apoptosis-associated signaling pathways.. The cardiomyocyte apoptosis was measured by fluorescein isothiocyanate conjugated annexin V/propidium iodide double staining cytometry, indicating that the percentage of early apoptotic cells increased from 15.6% +/- 2.6% to 25.5% +/- 2.5% in control and 20-HETE-treated cells, respectively. The mitochondrial membrane potential ([DELTA][PSI]m) was measured by detecting the ratio of JC-1 green/red emission intensity. A significant decrease in the ratio was observed after treatment with 20-HETE for 24 hours in comparison with control group, suggesting the disruptive effect of 20-HETE on mitochondrial [DELTA][PSI]m. In addition, 20-HETE stimulated caspase-3 activity and Bax mRNA expression in cardiomyocytes. In contrast, the Bcl-2 mRNA levels were significantly decreased by 20-HETE treatment.. These results demonstrate that 20-HETE induces cardiomyocyte apoptosis by activation of several intrinsic apoptotic pathways. The 20-HETE-induced apoptosis could contribute to the cytochrome P450 [omega]-hydroxylase-dependent cardiac injure during cardiac ischemia-reperfusion.

Topics: Amidines; Animals; Animals, Newborn; Apoptosis; Arachidonic Acid; bcl-2-Associated X Protein; Benzimidazoles; Carbocyanines; Caspase 3; Cell Survival; Cytochrome P-450 CYP4A; Cytochrome P-450 Enzyme Inhibitors; Cytochrome P-450 Enzyme System; Fluorescent Dyes; Genes, bcl-2; Hydroxyeicosatetraenoic Acids; Hydroxylation; Membrane Potential, Mitochondrial; Mitochondria; Myocytes, Cardiac; Rats; Rats, Wistar; Signal Transduction; Staining and Labeling

2011