Ferroptosis participated in hippocampal neuroinflammation damage of in offspring rats after maternal sleep deprivation

Sleep deprivation during pregnancy has important effects on the pregnant woman herself and her offspring, and some studies have found that neuroinflammation in her offspring is important, but the mechanisms are poorly understood. To investigate the involvement of ferroptosis in cognitive impairment due to hippocampal neuroinflammation in offspring rats after maternal sleep deprivation. SD rats exposed to late gestational sleep deprivation were deprived of sleep for 72 h. Their offspring were given the ferroptosis inhibitor liproxstatin-1 (5 mg/kg) intraperitoneally 3 days after birth. The results showed that MSD resulted in impaired learning memory capacity and significant downregulation of PSD95 and NeuN. Microglia were significantly activated, inflammatory factor expression was increased, the ferroptosis regulatory protein GPX4 was downregulated, ACSL4 was significantly upregulated, and lipid metabolite 4-HNE expression was increased. In contrast, the MSD-induced impairment of inflammation and learning memory capacity in the offspring was ameliorated after treatment with ferroptosis inhibitors. These results suggest that MSD-induced neural damage characterized ferroptosis in the hippocampal region of the offspring rats, leading to a decrease in learning and memory function, which may be related to the decreased levels of Nrf2 and HO-1.