Remifentanil alleviates hypoxic-ischemic brain damage-induced cognitive impairment via BACH1.

Hypoxia-ischemia (HI) is among the most frequent causes of death and disability in neonates. We aimed here to examine the neuroprotective effects of Remifentanil (RE) and the underlying mechanisms in a rat model of hypoxic-ischemic brain damage (HIBD). We found that RE improved the learning memory ability, reduced neuronal cell damage and apoptosis, reduced inflammation induced by suppressing the expression of BTB domain and CNC homolog 1 (BACH1) in rats with HIBD. BACH1 attenuated the alleviating effect of RE on cognitive impairment in HIBD rats. Moreover, RE inhibited TRAF3 expression by downregulating BACH1, and TRAF3 attenuated the therapeutic effect of RE on cognitive impairment by activating the NF-κB signaling. In conclusion, our findings demonstrated that RE inhibits the expression of BACH1, which in turn inhibits the NF-κB signaling pathway by suppressing TRAF3. RE may be a promising therapeutic agent to attenuate HIBD-induced cognitive impairment.