title: A cocaine-regulated and amphetamine-regulated transcript inhibits oxidative stress in neurons deprived of oxygen and glucose.
abstract: Stroke, of which about 87% is ischemic stroke, constitutes one of the main causes of morbidity, disability, and mortality worldwide. Ischemic brain injury has complex pathological mechanisms. Considerable evidence has been collected over the last few years suggesting that oxidative stress associated with excessive production of reactive oxygen species is a fundamental mechanism of brain damage in stroke and reperfusion after stroke. Oxidative stress is an important trigger of neuronal apoptosis in ischemic stroke. In this current study, it was found that cocaine-regulated and amphetamine-regulated transcript 55-102 (CART55-102) inhibited oxygen-induced and glucose deprivation (OGD)-induced neurotoxicity in a dose-dependent manner. The peak dose of CART55-102 was 0.4 nmol/l. In addition, the level of intracellular reactive oxygen species was decreased in OGD-treated neurons in the presence of 0.4 nmol/l CART55-102. Mitochondrial membrane potential (ΔΨm) and mtDNA mRNA expressions were increased in OGD-treated neurons in the presence of 0.4 nmol/l CART55-102. The current study suggests that CART55-102, by inhibiting oxidative stress, may be developed into therapeutic agents for ischemic stroke.
authors.affiliation: Department of Neurology, Nanjing Drum Tower Hospital-Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
authors.forename: Dujuan
authors.initials: D
authors.lastname: Sha
authors.forename: Zhongyuan
authors.initials: Z
authors.lastname: Wang
authors.forename: Lai
authors.initials: L
authors.lastname: Qian
authors.forename: Yong
authors.initials: Y
authors.lastname: Han
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.forename: Shuangshuang
authors.initials: S
authors.lastname: Gu
authors.forename: Luna
authors.initials: L
authors.lastname: Wang
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Cong
authors.initials: C
authors.lastname: Chen
authors.forename: Yun
authors.initials: Y
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015687:Cell Hypoxia / Q000502:physiology*; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D004396:Coloring Agents; D005434:Flow Cytometry; D005947:Glucose / Q000172:deficiency* / Q000502:physiology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000494:pharmacology*; D009474:Neurons / Q000502:physiology*; D018384:Oxidative Stress / Q000235:genetics / Q000502:physiology*; D010446:Peptide Fragments / Q000494:pharmacology*; D061251:Primary Cell Culture; D017382:Reactive Oxygen Species; D060888:Real-Time Polymerase Chain Reaction; D013778:Tetrazolium Salts; D013844:Thiazoles; D000098882:Cocaine- and Amphetamine-Regulated Transcript Protein
chemical_list: D004396:Coloring Agents; D005947:Glucose; D009419:Nerve Tissue Proteins; D010446:Peptide Fragments; D017382:Reactive Oxygen Species; D013778:Tetrazolium Salts; D013844:Thiazoles; C428723:cocaine- and amphetamine-regulated transcript protein (55-102); D000098882:Cocaine- and Amphetamine-Regulated Transcript Protein; C022616:thiazolyl blue