Atractylon treatment prevents sleep-disordered breathing-induced cognitive dysfunction by suppression of chronic intermittent hypoxia-induced M1 microglial activation

Chronic intermittent hypoxia (CIH) induced by sleep-disordered breathing (SDB) is a key factor involved in cognitive dysfunction (CD). Increasing evidence has shown that atractylon (ATR) has anti-inflammatory effects. However, it remains unclear if ATR has a protective effect against SDB-induced nerve cell injury and CD. So, in the present study, CIH-exposed mice and CIH-induced BV2 cells were used to mimic SDB. The results showed that ATR treatment decreased CIH-induced CD and the expression of inflammatory factors in the hippocampal region by suppression of M1 microglial activation and promotion of M2 microglial activation. Also, ATR treatment promoted sirtuin 3 (SIRT3) expression. Down-regulation of SIRT3 decreased the protective effect of ATR against CIH-induced microglial cell injury. Furthermore, in vitro detection found that SIRT3 silencing suppressed ATR-induced M2 microglial activation after exposure to CIH conditions. Taken together, these results indicate that ATR treatment prevents SDB-induced CD by inhibiting CIH-induced M1 microglial activation, which is mediated by SIRT3 activation.