Post-Ischemic Treatment with Sevoflurane: To Reduce Myocardial Ischemic/Reperfusion Injury in Rats by miR-26a-5p/PTEN/PI3K/Akt Signaling Pathway
Post-Ischemic Treatment with Sevoflurane: To Reduce Myocardial Ischemic/Reperfusion Injury in Rats by miR-26a-5p/PTEN/PI3K/Akt Signaling Pathway
Shaolin Zeng, Shuai Yuan* and Kai Liu
ABSTRACT
The aim of the study was to determine the effect of sevoflurane on myocardial ischemic/reperfusion (I/R) injury in rats and its causative role. The differential expressions of miRNA in the rat myocardial tissue after post-ischemic treatment with sevoflurane were screened by miRNA expression profile chip. The potential targets of miR-26a-5p were predicted by application of Targetscan, microT-CDS, miRtargetLink and miRpathDB database. The luciferin reporter groups were used for verification. We detected the impact of miR-26a-5p expression content on the PTEN/PI3K/Akt pathway via Western blot. We used HE staining for examining how miR-26a-5p expression content affected myocardium morphology of rats in the sevoflurane group, Biochemical experiments for assessing how miR-26a-5p expression content affected myocardial tri-enzymes in the sevoflurane group, as well as Western blot for evaluating how miR-26a-5p expression content affects apoptosis of rats in the sevoflurane group. The impact of miR-26a-5p expression content on levels of oxidative stress indicators of myocardial tissue of rats in the sevoflurane group was detected by ELISA. We found that the inhibition expressed by content of miR-26a-5p in rats after post-ischemic treatment with sevoflurane inhibited the anti-inflammatory effect of post-ischemic treatment with sevoflurane. The post-ischemic treatment with sevoflurane promoted the activity of SOD, CAT as well as GSH-Px, and inhibited MDA and ROS levels, while miR-26a-5p inhibition expression content inhibited the increase in activity of SOD. To conclude, the post-ischemic treatment with sevoflurane is able to inhibit PTEN expression to promote the activation of PI3K/Akt signaling pathway by increase in miR-26a-5p expression level, thereby playing a role in resisting myocardial ischemia/reperfusion damage.
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