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[Protective effects of nitric oxide donor on hydrogen peroxide-induced injury of cardiomyocytes].
Sheng Li Xue Bao. 2004 Aug 25; 56(4):481-6.SL

Abstract

To investigate the protective effects of nitric oxide (NO) on cardiomyocytes against hydrogen peroxide (H2O2)-induced injury, cultured neonatal cardiomyocytes were divided into three groups: (1) normal group; (2) H2O2 group: cells were treated with H2O2 (0.1 mmol/L) for 4 h; (3) SNAP+ H2O2 group: cells were pretreated with NO donor S-nitroso-N-acetyl-1,1-penicillamine (SNAP, 0.5 mmol/L) 10 min before H2O2 treatment. Colorimetric assay was used to detect cell viability and lactate dehydrogenase (LDH) activity to evaluate cell injury. Apoptotic rate of cardiomyocytes were determined by flow cytometer. Superoxide dismutase (SOD) activity and malonaldehyde (MDA) content were measured by colorimetric assay to evaluate cell antioxidant ability. Intracellular calcium was tested by laser confocal microscopy. The results showed that after treatment with H2O2, cell viability was significantly reduced to 58.3+/-7.6% compared with normal group (93.1+/-6.2 %). LDH activity and apoptotic rates were 1580.5+/-186.7 U/L and 26.4+/-5.7% respectively, significantly higher than that of normal group (631.4+/-75.6 U/L and 0). SNAP pretreatment markedly improved cell viability to 79.7+/-9.3% and reduced LDH activity and apoptotic rates to 957.8+/-110.9 U/L and 9.1+/-3.3%, respectively. Cells treated with H2O2 had a lower SOD activity of 14.73+/-1.68 NU/ml and a higher MDA content of (15.35+/-3.49) micromol/L compared with normal cells (19.67+/-0.85 NU/ml) and (6.95+/-0.83 micromol/L), respectively. Cells with SNAP pretreatment had a higher SOD activity of 21.36+/-3.11 NU/ml and a lower MDA content of 9.12+/-1.47 micromol/L compared with H2O2 group. Intracellular calcium content was reduced by SNAP administration while enhanced by H2O2. Pretreatment with SNAP could antagonize the effect of H2O2 of accelerating intracellular calcium content. Based on the results observed, it is concluded that NO donor SNAP may protect cardiomyocytes from being injured by H2O2. The underlying mechanisms may include improving cell antioxidant ability and reducing intracellular calcium overload.

Authors+Show Affiliations

Department of Pharmacology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

15322683

Citation

Zhang, Feng, et al. "[Protective Effects of Nitric Oxide Donor On Hydrogen Peroxide-induced Injury of Cardiomyocytes]." Sheng Li Xue Bao : [Acta Physiologica Sinica], vol. 56, no. 4, 2004, pp. 481-6.
Zhang F, Zhang T, Zhu XX, et al. [Protective effects of nitric oxide donor on hydrogen peroxide-induced injury of cardiomyocytes]. Sheng Li Xue Bao. 2004;56(4):481-6.
Zhang, F., Zhang, T., Zhu, X. X., Liu, L. N., Li, C., & Mei, Q. B. (2004). [Protective effects of nitric oxide donor on hydrogen peroxide-induced injury of cardiomyocytes]. Sheng Li Xue Bao : [Acta Physiologica Sinica], 56(4), 481-6.
Zhang F, et al. [Protective Effects of Nitric Oxide Donor On Hydrogen Peroxide-induced Injury of Cardiomyocytes]. Sheng Li Xue Bao. 2004 Aug 25;56(4):481-6. PubMed PMID: 15322683.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Protective effects of nitric oxide donor on hydrogen peroxide-induced injury of cardiomyocytes]. AU - Zhang,Feng, AU - Zhang,Tao, AU - Zhu,Xiao-Xing, AU - Liu,Lin-Na, AU - Li,Chen, AU - Mei,Qi-Bing, PY - 2004/8/24/pubmed PY - 2005/8/17/medline PY - 2004/8/24/entrez SP - 481 EP - 6 JF - Sheng li xue bao : [Acta physiologica Sinica] JO - Sheng Li Xue Bao VL - 56 IS - 4 N2 - To investigate the protective effects of nitric oxide (NO) on cardiomyocytes against hydrogen peroxide (H2O2)-induced injury, cultured neonatal cardiomyocytes were divided into three groups: (1) normal group; (2) H2O2 group: cells were treated with H2O2 (0.1 mmol/L) for 4 h; (3) SNAP+ H2O2 group: cells were pretreated with NO donor S-nitroso-N-acetyl-1,1-penicillamine (SNAP, 0.5 mmol/L) 10 min before H2O2 treatment. Colorimetric assay was used to detect cell viability and lactate dehydrogenase (LDH) activity to evaluate cell injury. Apoptotic rate of cardiomyocytes were determined by flow cytometer. Superoxide dismutase (SOD) activity and malonaldehyde (MDA) content were measured by colorimetric assay to evaluate cell antioxidant ability. Intracellular calcium was tested by laser confocal microscopy. The results showed that after treatment with H2O2, cell viability was significantly reduced to 58.3+/-7.6% compared with normal group (93.1+/-6.2 %). LDH activity and apoptotic rates were 1580.5+/-186.7 U/L and 26.4+/-5.7% respectively, significantly higher than that of normal group (631.4+/-75.6 U/L and 0). SNAP pretreatment markedly improved cell viability to 79.7+/-9.3% and reduced LDH activity and apoptotic rates to 957.8+/-110.9 U/L and 9.1+/-3.3%, respectively. Cells treated with H2O2 had a lower SOD activity of 14.73+/-1.68 NU/ml and a higher MDA content of (15.35+/-3.49) micromol/L compared with normal cells (19.67+/-0.85 NU/ml) and (6.95+/-0.83 micromol/L), respectively. Cells with SNAP pretreatment had a higher SOD activity of 21.36+/-3.11 NU/ml and a lower MDA content of 9.12+/-1.47 micromol/L compared with H2O2 group. Intracellular calcium content was reduced by SNAP administration while enhanced by H2O2. Pretreatment with SNAP could antagonize the effect of H2O2 of accelerating intracellular calcium content. Based on the results observed, it is concluded that NO donor SNAP may protect cardiomyocytes from being injured by H2O2. The underlying mechanisms may include improving cell antioxidant ability and reducing intracellular calcium overload. SN - 0371-0874 UR - https://www.unboundmedicine.com/medline/citation/15322683/[Protective_effects_of_nitric_oxide_donor_on_hydrogen_peroxide_induced_injury_of_cardiomyocytes]_ L2 - http://www.actaps.com.cn/paper/200404/481.pdf DB - PRIME DP - Unbound Medicine ER -