Title: Role of NF-κB/I-κB in cardiomyocyte injury induced by hydrogen peroxide
Abstract:Objective:This study was designed to investigate the role of NF-κB/I-κB in cardiomyocyte injury during the oxidative stress. Methods:Injury of neonatal rat cardiomyocytes was induced by exposure to 0....Objective:This study was designed to investigate the role of NF-κB/I-κB in cardiomyocyte injury during the oxidative stress. Methods:Injury of neonatal rat cardiomyocytes was induced by exposure to 0.5 mmol/L hydrogen peroxide (H 2O 2) for different durations. Cardiomyocyte necrosis and apoptosis were determined by cell death rate, LDH release rate and terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling (TUNEL) respectively. The change of I-κB was assayed by Western Blot. The translocation of NF-κ B from cytoplasm to nucleus was observed by immunohistochemical analysis. Results: Exposure to 0.5 mmol/L H 2O 2 resulted in neonatal ratcardiomyocyte necrosis and apoptosis as shown by increase of cell death rate, LDH release rate and TUNEL positivity respectively. Level of I-κB,an endogenous inhibitory protein of NF-κB, began to decrease after 5 min of H 2O 2 treatment, reached nadir at 15 min, and recovered at 1 h. The translocation of NF-κB from cytoplasm to nucleus in cardiomyocytes was observed after exposure to H 2O 2 for 0.5 h. Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB, could attenuate H 2O 2-induced increase of LDH release rate in cardiomyocyte ( P 0.01). Conclusion:H 2O 2 could induce both necrosis and apoptosis of cultured neonatal rat cardiomyocytes,which could be mediated by activation of NF-κB/I-κB pathway.Read More
Publication Year: 2004
Publication Date: 2004-01-01
Language: en
Type: article
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