Format

Send to

Choose Destination
Brain Res. 2014 Sep 25;1582:107-13. doi: 10.1016/j.brainres.2014.07.043. Epub 2014 Aug 13.

Cocaine- and amphetamine-regulated transcript peptide increases mitochondrial respiratory chain complex II activity and protects against oxygen-glucose deprivation in neurons.

Author information

1
Department of Emergency, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, Nanjing 210008, Jiangsu Province, China; Department of Emergency, Drum Tower Clinical Medical School, Nanjing Medical University, Nanjing 210008, Jiangsu Province, China; The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.
2
Department of Emergency, Drum Tower Clinical Medical School, Nanjing Medical University, Nanjing 210008, Jiangsu Province, China.
3
Department of Neurology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, 321 Zhongshan Road, Nanjing 210008, Jiangsu Province, China; The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.
4
Department of Emergency, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, Nanjing 210008, Jiangsu Province, China; The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.
5
Department of Neurology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, 321 Zhongshan Road, Nanjing 210008, Jiangsu Province, China; The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China. Electronic address: 13951980866@139.com.

Abstract

The mechanisms of ischemic stroke, a main cause of disability and death, are complicated. Ischemic stroke results from the interaction of various factors including oxidative stress, a key pathological mechanism that plays an important role during the acute stage of ischemic brain injury. This study demonstrated that cocaine- and amphetamine-regulated transcript (CART) peptide, specifically CART55-102, increased the survival rate, but decreased the mortality of neurons exposed to oxygen-glucose deprivation (OGD), in a dose-dependent manner. The above-mentioned effects of CART55-102 were most significant at 0.4nM. These results indicated that CART55-102 suppressed neurotoxicity and enhanced neuronal survival after oxygen-glucose deprivation. CART55-102 (0.4nM) significantly diminished reactive oxygen species levels and markedly increased the activity of mitochondrial respiratory chain complex II in oxygen-glucose deprived neurons. In summary, CART55-102 suppressed oxidative stress in oxygen-glucose deprived neurons, possibly through elevating the activity of mitochondrial respiratory chain complex II. This result provides evidence for the development of CART55-102 as an antioxidant drug.

KEYWORDS:

Cocaine- and amphetamine-regulated transcript peptides; Mitochondrial respiratory chain; Neuroprotection; Oxygen–glucose deprivation; Reactive oxygen species

PMID:
25128463
DOI:
10.1016/j.brainres.2014.07.043
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center