Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Stroke Cerebrovasc Dis. 2014 Feb;23(2):303-9. doi: 10.1016/j.jstrokecerebrovasdis.2013.02.020. Epub 2013 Mar 27.

The effect of mitochondrial calcium uniporter opener spermine on diazoxide against focal cerebral ischemia--reperfusion injury in rats.

Author information

  • 1Department of Anesthesiology of Liaocheng People's Hospital, The Medical College of Qingdao University, Qingdao, Shandong Province, China.
  • 2Department of Anesthesiology of Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong Province, China. Electronic address: wshlei@yahoo.com.cn.

Abstract

BACKGROUND:

Recent research has indicated that mitochondrial adenosine triphosphate-sensitive potassium channels play an important role in cerebral protection, which involves in attenuating the calcium of mitochondria. However, the effect of diazoxide on cerebral ischemia-reperfusion and the role of spermine, the agonist of mitochondrial calcium uniporter (MCU), remain unknown.

OBJECTIVE:

We investigated the effect of MCU opener spermine on diazoxide against focal cerebral ischemia-reperfusion injury in rats.

METHODS:

Adult male Wistar rats were randomly divided into 5 groups: the Sham group, the I/R group, the Dzx + I/R group, the Dzx + Sper + I/R group, and the Sper + I/R group. Rats were exposed to 2-hour ischemia and 24-hour reperfusion. Diazoxide were administrated 30 minutes before ischemia, and spermine were given 10 minutes before reperfusion. Rats in the Sham group did not experience the process of ischemia-reperfusion. After 24-hour reperfusion, rats were given neurological performance tests, overdosed with general anesthesia, and then their brains were excised for infarct volume, pathological changes, and biochemical evaluation and analysis.

RESULTS:

Rats in the Dzx + I/R group displayed improved neurological deficits and decreased infarct volume and oxidative stress (evidenced by decreased nitric oxide and malondialdehyde but increased antioxidant enzymes [eg, glutathione peroxide and superoxide dismutase]) caused by ischemia-reperfusion. The beneficial effects of diazoxide were significantly attenuated by spermine treatment. Rats in the Sper + I/R group displayed worse neurological deficits, larger infarct volume and more oxidative stress, and less antioxidant enzymes than those in the Dzx + I/R.

CONCLUSIONS:

Our results suggested that diazoxide, which improved neurological deficits and decreased infarct volume and oxidative stress against ischemia-reperfusion injury, is mediated by spermine.

Copyright © 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.

KEYWORDS:

Nitric oxide; antioxidative enzymes; lipid peroxidation; mitochondrial uniporter

PMID:
23540254
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk