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Histamine H2-Receptor Antagonist Ranitidine Protects Against Neural Death Induced by Oxygen-Glucose Deprivation

Histamine H2-Receptor Antagonist Ranitidine Protects Against Neural Death Induced by Oxygen-Glucose Deprivation. Malagelada, Cristina; Xifro, Xavier; Badiola, Nahuai; Sabria, Josefa; Rodriguez-Alvarez, Jose (Institut de Neurociences and Unitat de Bioquimica de Medicina, Departament de Bioquimica i Biologia Molecular, Universitat Autonoma de Barcelona, Spain). Stroke, 35(10), 2396-2401 (English) 2004 Lippincott Williams & Wilkins. CODEN: SJCCA7. ISSN: 0039-2499. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Background and Purpose: Administration of histamine receptor antagonists has been reported to produce contradictory results, either reducing or increasing neural damage induced by ischemia. In this study, we investigated the neuroprotective effects of histamine H2-receptor antagonists in an "in vitro" model of ischemia. Methods: Cultured rat brain cortical neurons were exposed to oxygen-glucose deprivation (OGD) in the presence or absence of different histaminergic drugs. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide redn. assay. Necrosis and apoptosis were quantified by staining cells with propidium iodide and Hoechst 33258. Caspase 3 activation was detd. by immunocytochem. and Western blot. Results: Pretreatment with H2 antagonists effectively reduced neuronal cell death induced by OGD. Ranitidine decreased the no. 142437-67-0 and 50-99-7 which are cas registry numbers of chemicals are mentioned. of necrotic and apoptotic cells. Caspase 3 activation and alteration of the neuronal cytoskeleton were also prevented by ranitidine pretreatment. The neuroprotective effect of ranitidine was still evident when added 6 h after OGD. Conclusions: H2-receptor antagonists protected against OGD-induced neuronal death. Ranitidine attenuated cell death even when administered after OGD. These data suggest that this drug, which is currently used for the treatment of gastric ulcers, may be useful in promoting recovery after ischemia. .