Acetylpuerarin inhibits oxygen-glucose deprivation-induced neuroinflammation of rat primary astrocytes via the suppression of HIF-1 signaling.

In the central nervous system (CNS), ischemic injury induced by inflammation associated with astrocytes serves an important role in physiological and pathological processes. Neuroinflammation leads to the release of pro-inflammatory cytokines, including tumor necrosis factor-α and interleukin-1β. The aim of the present study was to investigate whether acetylpuerarin attenuates oxygen-glucose deprivation (OGD)-induced astrocyte inflammation and secretion of pro-inflammatory cytokines via inhibiting hypoxia-inducible factor-1 (HIF-1) activation and suppressing downstream primary astrocyte signaling in rats. The results demonstrated that acetylpuerarin attenuates astrocyte viability and induces morphological changes following OGD stress. Furthermore, acetylpuerarin suppresses the stimulation of HIF-1α and nuclear factor (NF)-κB signaling pathways, while attenuating the expression and secretion of pro-inflammatory cytokines via HIF-1 suppression in OGD-induced astrocytes. These findings indicate that acetylpuerarin may attenuate OGD-induced astrocyte damage and inflammation in rat primary astrocytes via suppressing HIF-1 activation and NF-κB signaling. These results suggest that acetylpuerarin regulates inflammation associated with astrocytes and may represent a novel therapeutic agent for the treatment of neuroinflammation in the CNS.