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Article Abstract
Post-stroke depression (PSD) is a common psychiatric complication that occurs after stroke, especially in ischemic stroke (I/S). It has been reported that high-mobility group box-1 (HMGB1) is highly expressed in clinical PSD patients, but the exact molecular mechanism of its involvement in PSD is not completely clear, the neuroinflammation may participate in its development. Thus, we established a PSD rat model, observed behavioral and cognitive deficits, and found that the HMGB1/ receptor for advanced glycation end products (RAGE) pathway were activated in microglia. Glycyrrhizin acid (GA), an inhibitor of HMGB1, inhibited microglial activation, reversed the expression of HMGB1/RAGE, and ameliorated depressive-like behaviors in PSD rats. GA also reduced the expression of MAPK and NF-κB, which further led to decreased expression of IL-1β and NLRP3 inflammasome. These results suggested that the HMGB1/RAGE pathway was involved in microglial activation in the PSD model, promoting neuroinflammation and depressive-like behaviors.
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