β2-Adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice
| العنوان: | β2-Adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice |
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| المؤلفون: | Loubna Erraji, Jesintha Gaston, Paule Varlet, Jean-Gérard Guillet, Claudine André, Dominique Couton, Laurent Rénia, Pascale Briand |
| المصدر: | American Journal of Physiology-Gastrointestinal and Liver Physiology. 276:G647-G654 |
| بيانات النشر: | American Physiological Society, 1999. |
| سنة النشر: | 1999 |
| مصطلحات موضوعية: | Agonist, Cell type, medicine.medical_specialty, Programmed cell death, Physiology, Ratón, medicine.drug_class, Adrenergic beta-Antagonists, Drug Resistance, Apoptosis, Mice, Transgenic, Stimulation, Biology, Mice, Physiology (medical), Internal medicine, Receptors, Adrenergic, beta, medicine, Animals, Clenbuterol, fas Receptor, Dose-Response Relationship, Drug, Hepatology, Gastroenterology, Antibodies, Monoclonal, Drug Synergism, Adrenergic beta-Agonists, Propranolol, Death, Mice, Inbred C57BL, Endocrinology, Liver, medicine.drug |
| الوصف: | Stimulation of the cAMP-signaling pathway modulates apoptosis in several cell types and inhibits Jo2-mediated apoptosis in cultured rat hepatocytes. No information is yet available as to whether the hepatic β2-adrenergic receptor (AR) expression level, including β2-AR-dependent adenylyl cyclase activation, modulates hepatocyte sensitivity to apoptosis in vivo or whether this sensitivity can be modified by β2-AR ligands. We have examined this using C57BL/6 mice, in which hepatic β2-AR densities are low, and transgenic F28 mice, which overexpress β2-ARs and have elevated basal liver adenylyl cyclase activity. The F28 mice were resistant to Jo2-induced liver apoptosis and death. The β-AR antagonist propranolol sensitized the F28 livers to Jo2. In normal mice clenbuterol, a β2-AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another β2-AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. This indicates that the expression level of functional β2-ARs modulates Fas-regulated liver apoptosis and that this apoptosis can be inhibited in vivo by giving β2-AR agonists. This may well form the basis for a new therapeutic approach to diseases involving abnormal apoptosis. |
| تدمد: | 1522-1547 0193-1857 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c293e1c03c5e556d89cbb431185eb095Test https://doi.org/10.1152/ajpgi.1999.276.3.g647Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....c293e1c03c5e556d89cbb431185eb095 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15221547 01931857 |
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