N-acetylcysteine treatment normalizes serum tumor necrosis factor-alpha level and hinders the progression of cardiac injury in hypertensive rats
| Autor: | Gabriele Candiani, C. Adamy, Marie-Claude Bourin, Sylviane Adubeiro, Jean-Luc Dubois-Randé, Michel Cailleret, Luc Hittinger, Françoise Roudot-Thoraval, Françoise Pecker, Thierry Badoual, Marie Bourraindeloup, Jin Bo Su |
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| Rok vydání: | 2004 |
| Předmět: |
Male
medicine.medical_treatment Drug Evaluation Preclinical Antioxidants Acetylcysteine chemistry.chemical_compound Ventricular Dysfunction Left Ultrasonography chemistry.chemical_classification biology Ventricular Remodeling Glutathione Nitric oxide synthase Cytokine NG-Nitroarginine Methyl Ester Sphingomyelin Phosphodiesterase Matrix Metalloproteinase 9 Hypertension Thiol Disease Progression Matrix Metalloproteinase 2 Tumor necrosis factor alpha Collagen Cardiology and Cardiovascular Medicine medicine.drug medicine.medical_specialty Sodium Heart Ventricles chemistry.chemical_element Nitric Oxide Physiology (medical) Internal medicine medicine Animals Rats Wistar Sodium Chloride Dietary business.industry Tumor Necrosis Factor-alpha Myocardium medicine.disease Myocardial Contraction Rats Oxidative Stress Endocrinology chemistry Heart failure biology.protein Nitric Oxide Synthase business |
| Zdroj: | Circulation. 110(14) |
| ISSN: | 1524-4539 |
| Popis: | Background— Studies in isolated cardiomyocytes showed that replenishment in cellular glutathione, achieved with the glutathione precursor N -acetylcysteine (NAC), abrogated deleterious effects of tumor necrosis factor-α (TNF-α). Methods and Results— We examined the ability of NAC to limit the progression of cardiac injury in the rat model of hypertension, induced by the nitric oxide synthase inhibitor N G -nitro- l -arginine methyl ester (L-NAME) (50 mg/kg per day SC) and high-salt diet (HS) (8% NaCl). Four-week HS/L-NAME administration induced hypertension (193±8 versus 122±4 mm Hg for low-salt diet [LS] group) and left ventricular (LV) dysfunction, revealed by echocardiography and characterized by decreased LV shortening fraction (38±2% versus 49±4% for LS group; P P Conclusions— These findings suggest that glutathione status determines the adverse effects of TNF-α in cardiac failure and that TNF-α antagonism may be achieved by glutathione supplementation. |
| Databáze: | OpenAIRE |
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