Post-stroke angiotensin II type 2 receptor activation provides long-term neuroprotection in aged rats.

摘要: Activation of the angiotensin II type 2 receptor (AT2R) by administration Compound 21 (C21), a selective AT2R agonist, induces neuroprotection in models ischemic stroke young adult animals. The mechanisms this neuroprotective action are varied, and may include direct indirect effects activation. Our objectives were to assess long-term protective post-stroke C21 treatments clinically-relevant model aged rats characterize cellular localization AT2Rs mouse brain transgenic reporter mice following stroke. Intraperitoneal injections (0.03mg/kg) after induced transient monofilament middle cerebral artery occlusion resulted that sustained for up at least 3-weeks post-stroke. These included improved neurological function across multiple assessments significant reduction infarct volume as assessed magnetic resonance imaging. We also found expression be on neurons, not astrocytes or microglia, normal female male brains. Stroke did induce altered when 7 14 days findings demonstrate previously characterized only during earlier time points using animals is rats, implying even greater clinical relevance study agonists acute treatment human disease. Further, it appears likely due mix both stemming from activation neurons other cells besides microglia.