Silencing of PTEN inhibits the oxidative stress damage and hippocampal cell apoptosis induced by Sevoflurane through activating MEK1/ERK signaling pathway in infant rats

Abstract

Phosphatase and tensin homolog (PTEN) is a suppressive player in tumor but its concrete role in oxidative stress (OS) damage and cell apoptosis remains much exploration. Thus, this study is conducted to explore the participation of PTEN and its mechanisms in OS damage and cell apoptosis in hippocampal cells. Infant rats were grouped into normal, Sevo, Sevo + si-negative control (NC), Sevo + si-PTEN and Sevo + si-PTEN + PD (MEK1/ERK signaling pathway inhibitor) groups. Infant hippocampal cells were grouped into blank, Sevo, Sevo + si-NC, Sevo + si-PTEN and Sevo + si-PTEN + PD groups. The expressions of PTEN and MEK1/ERK signaling pathway-related proteins were determined. OS-related indices in hippocampal tissues and cells were detected. Cell apoptosis was detected by flow cytometry. Sevoflurane up-regulated PTEN expression and silencing of PTEN activates MEK1/ERK signaling pathway in hippocampal tissues and cells of infant rats. Silencing of PTEN alleviated hippocampal tissue pathological status and inhibited sevoflurane-induced cell apoptosis in hippocampal tissues of infant rats. Silencing of PTEN alleviated OS damage in hippocampal tissues of infant rats. Silencing of PTEN inhibited sevoflurane-induced apoptosis after OS damage in hippocampal cells of infant rats. Silencing of PTEN reduced sevoflurane-induced OS damage in hippocampal cells of infant rats. Our study demonstrates that PTEN silencing inhibits the OS damage and cell apoptosis in hippocampal cells induced by Sevoflurane through activating MEK1/ERK signaling pathway in infant rats.