Neuroprotection effect of quercetin on TNF-α levels and gene expression of caspase 3 in MPTP-Induced Male NMRI Mice

Abstract EN

Background: Apoptosis is a programmed cell death that occurs due to various factors such as reperfusion ischemia.

As a purinergic receptor, A1AR acts as an oxidative stress sensor and an antioxidant during reperfusion ischemia.

Objectives: The purpose of the present study was to investigate the effect of adenosine injection following cerebral reperfusion ischemia on A1AR gene expression and apoptosis in the brain hippocampal tissue of male Wistar rats.

Methods: This experimental study was conducted at Shahid Mirghani Research Institute in Gorgan, Iran, from January 21, 2019, to March 18, 2019.

The sample size was determined according to previous studies and a pilot study.

Thus, 30 male Wistar rats were divided into three groups by simple random sampling (using a random-number table): Control group (n = 10), Reperfusion ischemia group (n = 10), and Reperfusion ischemia + adenosine group (n = 10).

Ischemia was induced in animals by closing the carotid artery for 45 min.

Adenosine was injected 24 h after ischemia.

We measured A1AR gene expression, SOD protein expression, and apoptosis by real-time PCR, immunohistochemistry, and the TUNEL method, respectively.

Results: The results showed that cerebral reperfusion ischemia significantly increased A1AR gene expression (596%) and apoptosis (378%) and decreased SOD protein expression (72%) compared to the control group (P < 0.001).

On the other hand, adenosine significantly reduced A1AR gene expression (46%) and apoptosis (69%) and increased SOD protein expression (94%) compared to the ischemic group (P < 0.001).

Conclusions: Ischemic brain reperfusion causes oxidative stress.

Also, adenosine injection seems to be effective in reducing oxidative stress and apoptosis induced by cerebral reperfusion ischemia.