Sulfur dioxide reduces hippocampal cells death and improves learning and memory deficits in rat model of transient global ischemia/reperfusion

Objective(s): According to recent the findings, sulfur dioxide (SO2) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO2 exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objec...

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Bibliographic Details
Main Authors: Fatemeh Zare Mehrjerdie, Ali Shoshtari, Fahimeh Mohseni, Hossein Khastar, Pirasteh Norouzi, Yasin Asadi, Masoumeh Dadkhah, Mehdi Khaksari
Format: Article
Language:English
Published: Mashhad University of Medical Sciences 2018-10-01
Series:Iranian Journal of Basic Medical Sciences
Subjects:
Online Access:http://ijbms.mums.ac.ir/article_11363_0a51c6c850dbc6eb337d4c9a8d4b037e.pdf
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Summary:Objective(s): According to recent the findings, sulfur dioxide (SO2) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO2 exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objective of the current study was to examine the neuroprotective impact of SO2 following global cerebral ischemia/reperfusion (I/R).Materials and Methods: Forty-eight male Wistar rats that weighed 260–300 g, were randomly allocated into 4 groups: sham group (n=12), I/R group (n=12), and I/R+SO2 groups (NaHSO3 and Na2SO3; 1:3 ratio; 5 and 10 µg/kg, respectively; for 3 days, n=12). Cerebral ischemia model was prepared by occlusion of both common carotid arteries for 20 min. Saline as a vehicle and SO2 donor at doses 5 µg/kg (intraperitoneally) were injected for 3 days after reperfusion. Four days after ischemia, the passive avoidance memory test was carried out in four groups, and after behavioral assessment, necrosis, apoptosis, and antioxidant enzyme analysis were carried out.Results: SO2 treatment could significantly improve memory impairments in rats with cerebral ischemia/reperfusion (I/R) (P
ISSN:2008-3866
2008-3874