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Abstract
Post-stroke cognitive impairment (PSCI) occurs in up to 48% of patients, is animportant contributor to long-term disability. Hypertension is a major risk factor forPSCI. Currently, PSCI has no approved treatments. After stroke, the pro-inflammatorymicroglia activation plays an important role in developing PSCI. Previously, we usedC21, a direct AT2R agonist, we discovered that C21 reduces the development of PSCI.However, the exact mechanism of the C21 is undetermined. In this study, we hypothesizethat AT2R stimulation by C21 decreases the activated microglial phenotype (M1) andelevates M2 microglial phenotype, causing an improvement in PSCI. We tested ourhypothesis has by measuring the level of the IL-1 and IL-4 in brain after stroke. Next,we investigated the direct effect of C21 treatment on microglia polarization in-vitro. We found that C21 treatment prevented the increase of IL-1 in brain tissue and prevented microglia polarization toward a M1-like phenotype.