Aspirin inhibits inducible nitric oxide synthase expression and tumour necrosis factor-α release by cultured smooth muscle cells
| Autor: | V. del Pozo, Carlos Lahoz, I. Millás, F. González-Fernández, L. Sánchez de Miguel, Jerónimo Farré, J. Gómez, L. Rico, Rondón García, A. Jiménez, Antonio J. López-Farré, S. Casado, E. Aceituno, T. de Frutos |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
medicine.medical_specialty
Aspirin Necrosis Vascular smooth muscle biology medicine.medical_treatment Clinical Biochemistry Interleukin General Medicine Biochemistry Nitric oxide Nitric oxide synthase chemistry.chemical_compound Endocrinology Cytokine chemistry Internal medicine medicine biology.protein Tumor necrosis factor alpha medicine.symptom medicine.drug |
| Zdroj: | European Journal of Clinical Investigation. 29:93-99 |
| ISSN: | 0014-2972 |
| DOI: | 10.1046/j.1365-2362.1999.00425.x |
| Popis: | BACKGROUND: Inflammatory related cardiovascular disease, i.e. cardiac allograft rejection, myocarditis, septic shock, are accompanied by cytokine production, which stimulates the expression of inducible nitric oxide (iNOS). MATERIALS AND METHODS: The aim of the present study was to examine whether anti-inflammatory doses of acetylsalicylic acid (aspirin) could regulate iNOS protein expression in bovine vascular smooth muscle cells (BVSMCs) in culture. RESULTS: Interleukin 1 beta (IL-1 beta, 0.03 U mL-1) induced nitric oxide release by BVSMCs. Aspirin inhibited nitric oxide release from IL-1 beta-stimulated BVSMCs in a dose-dependent manner. In addition, aspirin significantly inhibited iNOS protein expression in BVSMCs and reduced the translocation of the nuclear factor-kappa B (NF-kappa B). Furthermore, aspirin and the blockade of NO generation by BVSMCs reduced the production of tumour necrosis factor alpha (TNF-alpha) by these cells. CONCLUSION: High doses of aspirin inhibited iNOS protein expression in BVSMCs and decreased NF-kappa B mobilization. The inhibition of iNOS expression by aspirin was further associated with a reduced ability of BVSMCs to produce TNF-alpha. This study could provide new mechanisms of action for aspirin in the treatment of the inflammation-related cardiovascular diseases. |
| Databáze: | OpenAIRE |
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