Artemisinin Alleviates Cerebral Ischemia/Reperfusion Injury via Regulation of the Forkhead Transcription Factor O1 Signaling Pathway

Abstract

The effect and mechanism of artemisinin therapy on cerebral ischemia-reperfusion injury (CIRI) was analyzed in this work. 100 healthy male C57BL/6 mice were selected and randomly divided into the sham group (no treatment), CIRI model group (IR), IR + artemisinin posttreatment group (IR + Arte), EX527 + IR group (EX527 + IR), and EX527 + IR + artemisinin posttreatment group (EX527 + IR + Arte), with 20 mice in each group. The cerebral infarct volumes of mice in different groups were measured by the 2,3,5-triphenyltetrazolium chloride (TTC) staining method. The neurological function scores and oxidative stress levels of mice in different groups were measured and compared. In addition, the expressions of silent information regulator 1 (SIRT1), forkhead transcription factor O1 (FOXO1), and p53 protein in brain tissue were detected. The results showed that the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) in the EX527 + IR group and EX527 + IR + Arte group were significantly higher than those in the IR + Arte group ( $P<0.05$ ). The expressions of SIRT1 protein in the brain tissue of the IR group and EX527 + IR group were much lower than that of the sham group ( $P<0.01$ ); compared with the IR + Arte group, the expression of the X527 + IR group in the brain tissue was greatly reduced ( $P<0.05$ ). The expression levels of FOXO1 protein and p53 protein in the brain tissue of mice in the IR group and EX527 + IR group were higher than those in the sham group ( $P<0.01$ ). It was concluded that artemisinin treatment can reduce oxidative stress damage and alleviate CIRI through the SIRT1/FOXO1 signaling pathway, thereby achieving neuroprotective effects.