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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.

SUBMITTER: Liu T

PROVIDER: S-EPMC7145332 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Type 2 diabetes (T2DM) and obesity are frequently associated with non-alcoholic fatty liver disease (NAFLD) and with an elevated cancer incidence. The molecular mechanisms of carcinogenesis in this context are only partially understood. High blood insulin levels are typical in early T2DM and excessive insulin can cause elevated reactive oxygen species (ROS) production and genomic instability. ROS are important for various cellular functions in signaling and host defense. However, elevated ROS formation is thought to be involved in cancer induction. In the molecular events from insulin receptor binding to genomic damage, some signaling steps have been identified, pointing at the PI3K/AKT pathway. For further elucidation Phosphatase and Tensin homolog (Pten), a tumour suppressor phosphatase that plays a role in insulin signaling by negative regulation of PI3K/AKT and its downstream targets, was investigated here. Dihydroethidium (DHE) staining was used to detect ROS formation in immortalized human hepatocytes. Comet assay and micronucleus test were performed to investigate genomic damage in vitro. In liver samples, DHE staining and western blot detection of HSP70 and HO-1 were performed to evaluate oxidative stress response. DNA double strand breaks (DSBs) were detected by immunohistostaining. Inhibition of PTEN with the pharmacologic inhibitor VO-OHpic resulted in increased ROS production and genomic damage in a liver cell line. Knockdown of Pten in a mouse model yielded increased oxidative stress levels, detected by ROS levels and expression of the two stress-proteins HSP70 and HO-1 and elevated genomic damage in the liver, which was significant in mice fed with a high fat diet. We conclude that PTEN is involved in oxidative stress and genomic damage induction in vitro and that this may also explain the in vivo observations. This further supports the hypothesis that the PI3K/AKT pathway is responsible for damaging effects of high levels of insulin.

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

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