Document Detail

Leptin administration alleviates ischemic brain injury in mice by reducing oxidative stress and subsequent neuronal apoptosis.
MedLine Citation:
PMID:  22491615     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Recent research has indicates that leptin plays a protective role in traumatic brain injury. We studied the protective effect of leptin on cerebral ischemia/reperfusion injury by using mice transient focal cerebral ischemia/reperfusion injury model.
METHODS: The distribution of 125I-leptin in the mouse brain was assessed by radioimmunoassay method. Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for two hours followed by 24 hours reperfusion. The neurologic deficits and infarct volume were determined using the Longa's score and 2,3,5-triphenyltetrazolium chloride staining, respectively. Regional cerebral blood flow was monitored by a laser-Doppler blood flowmeter. The levels of malondialdehyde, nitric oxide, nitric oxide synthase, and superoxide dismutase were detected according to respective assay kit. The histologic changes and neuronal apoptosis were observed with hematoxylin and eosin and transferase-mediated dUTP-biotin nick end labeling staining, respectively. The expression of B-cell lymphoma/leukemia-2 (Bcl-2) and cysteineasparateprotease-3 (caspase-3) were investigated by Western blot and real-time polymerase chain reaction assay.
RESULTS: Leptin decreased infarct volume and neurologic defects and improved regional cerebral blood flow and microvascular branch blood flow after injury. The malondialdehyde and nitric oxide levels were reduced, and superoxide dismutase level was increased after leptin treatment, which also minimized histologic changes and neuronal apoptosis, led to the upregulation of Bcl-2 and downregulation of caspase-3 expression after injury.
CONCLUSIONS: Peripherally administered leptin crossed the blood-brain barrier and was distributed into multiple regions of the brain; in the brain, leptin directly alleviated the injury-evoked damages by reducing oxidative stress and neuronal apoptosis.
Jin-Ying Zhang; Yi-Ling Si; Jie Liao; Guang-Tao Yan; Zi-Hui Deng; Hui Xue; Lu-Huan Wang; Kai Zhang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The journal of trauma and acute care surgery     Volume:  72     ISSN:  2163-0763     ISO Abbreviation:  J Trauma Acute Care Surg     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-04-11     Completed Date:  2012-06-27     Revised Date:  2013-09-25    
Medline Journal Info:
Nlm Unique ID:  101570622     Medline TA:  J Trauma Acute Care Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  982-91     Citation Subset:  AIM; IM    
Research Laboratory of Biochemistry, Basic Medical Institute, Basic Medical Institute, Chinese General Hospital of PLA, 28 Fuxing Road, Beijing 100853, People's Republic China.
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MeSH Terms
Apoptosis / drug effects*
Brain Chemistry / drug effects
Brain Ischemia / drug therapy*,  metabolism
Cerebral Infarction / drug therapy,  metabolism
Cerebrovascular Circulation / drug effects
Disease Models, Animal
Leptin / pharmacology*
Malondialdehyde / analysis
Nitric Oxide / analysis
Nitric Oxide Synthase / metabolism
Oxidative Stress / drug effects*
Superoxide Dismutase / metabolism
Reg. No./Substance:
0/Leptin; 10102-43-9/Nitric Oxide; 542-78-9/Malondialdehyde; EC Oxide Synthase; EC Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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