# Function and mechanism of the human SOD2 gene in mice cerebral ischemia/ reperfusion injury

## TL;DR

This study explores how the SOD2 gene protects the brain in mice after a stroke and how fenofibrate enhances this protection.

## Contribution

The study demonstrates that fenofibrate's neuroprotective effect is linked to increased SOD2 expression in a mouse model of cerebral ischemia.

## Key findings

- SOD2 transgenic mice showed significantly higher SOD2 expression in multiple organs compared to wild type mice.
- Fenofibrate treatment reduced infarct volume and improved blood flow recovery in wild type mice after ischemia reperfusion.
- SOD2 transgenic mice had reduced infarction volume regardless of treatment, suggesting SOD2's protective role.

## Abstract

To investigate the neuroprotective effects of the SOD2 gene in cerebral ischemia reperfusion injury function and the underlying mechanisms in a mice model of middle cerebral artery ischemia reperfusion.

SOD2 transgenic mice were engineered using transcription activator-like effector nucleases, and the genotype was identified using PCR after every three generations. Transgenic and C57BL/6J wild type mice were simultaneously subjected to the middle cerebral artery occlusion model.

SOD2 expression in the brain, heart, kidney, and skeletal muscle of transgenic mice was significantly higher than that in the wild type. Following ischemia reperfusion, the infarct volume of wild type mice decreased after treatment with fenofibrate compared to the CMC group. Infarction volume in SOD2 transgenic mice after CMC and fenofibrate treatment was significantly reduced. The recovery of cerebral blood flow in wild type mice treated with fenofibrate was significantly enhanced compared with that in the CMC group.

The expression of SOD2 in transgenic mice was significantly higher than that in wild type mice, the neuroprotective role of fenofibrate depends on an increase in SOD2 expression.