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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Antioxidants, Body Weight, Brain, Brain Infarction, Cresols, Disease Models, Animal, Dose-Response Relationship, Drug, Estradiol, Hormones, Infarction, Middle Cerebral Artery, Male, Memantine, Mice, Inbred C57BL, Motor Activity, Neuroprotective Agents.
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Is the neuroprotective effect of 17β-estradiol independent of its antioxidative properties? Context: 17β-Estradiol (E2) is neuroprotective in experimental models of stroke. While some postulate a mainly antioxidative action due to E2׳s free C3 hydroxyl group at its A-ring, others suggest that neuroprotection is mediated by a hormonal, receptor mediated effect. The aim of the current study was to clarify this issue by testing whether E2 analogues lacking hormonal activity are also neuroprotective following cerebral ischemia. Focal cerebral ischemia was induced in male C57/BL6 mice by laser-Doppler-controlled endovascular occlusion of the middle cerebral artery for 40min. Mice received either 1) memantine, a NMDA-receptor antagonist, as a positive control, 2) E2 (1400µg/kg b.w.), or 3) 2,4,6-trimethylphenol (TMP), an E2 analogue without hormonal activity (1400, 140, or 14µg/kg b.w.). Motor function was tested 3h and 24h after ischemia. Thereafter mice were sacrificed and brain damage was quantified by histomorphometry. Treatment with memantine or E2 significantly reduced infarct volume by >40% and significantly improved neurological function while treatment with TMP had no effect.
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E2 is equally neuroprotective as antagonization of NMDA receptors while E2 analogues without hormonal activity are not neuroprotective. Therefore the current data suggest that the neuroprotection activity of E2 is independent of its free-radical scavenging properties. Final Decision: yes