Echinacoside alleviates sevoflurane-induced cognitive dysfunction by activating FOXO1-mediated autophagy.

Abstract

The current study aimed to examine the effects of echinacoside on cognitive impairment in mice after exposure to sevoflurane. To examine the role of FOXO1, si-FOXO1 and si-con were injected into the hippocampus through the left lateral cerebral ventricles. Sevoflurane-induced mice had serious cognitive dysfunction. However, pretreatment with echinacoside alleviated the cognitive dysfunction, as measured by a shortened escape latency time, and increased platform crossing times, the percentage of distance in the target quadrant and Y-maze spontaneous alternations. In addition, we found that echinacoside elevated FOXO1 expression in the hippocampus; increased the expression of autophagy-related proteins including Beclin 1, ATG5, ATG7, and LC3; and reduced P62 expression. Silencing of FOXO1 aggravated the cognitive deficits and reduced expression of the autophagy-related markers, whereas the effects of si-FOXO1 on memory were abrogated by echinacoside. Echinacoside attenuated the cognitive impairment in sevoflurane-induced mice through FOXO1-mediated autophagy.