Document Detail


Forced, moderate-intensity treadmill exercise suppresses apoptosis by increasing the level of NGF and stimulating phosphatidylinositol 3-kinase signaling in the hippocampus of induced aging rats.
MedLine Citation:
PMID:  19524110     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
While nerve growth factor (NGF) activates various signaling cascades, the phosphatidylinositol 3-kinase (PI3-K)/Akt pathway plays a pivotal role in controlling the survival of neurons, although this activity declines during the aging process. We investigated the effect of forced moderate-intensity treadmill exercise on the level of NGF and the PI3-K/Akt signaling pathway in the hippocampus of induced aging rats. Forty-five male Sprague-Dawley rats were divided into the following three groups: (1) control group, in which aging was not induced (CON: n=15), (2) aging-control group, in which aging was induced but the rats were not subjected to exercise (ACON: n=15), and (3) the aging-exercise group, in which aging was induced and the rats were subjected to treadmill exercise (AEX: n=15). d-Galactose (50mg/kg) was injected into the abdominal cavity for 8 weeks to induce aging. Rats were subjected to treadmill exercise 5 days a week for 8 weeks, and the speed of the treadmill was gradually increased. The protein levels of NGF, P-PI3-K, and P-Akt were significantly high in the AEX group (p<0.01, p<0.01, and p<0.001, respectively). Tyrosine kinase A (Trk A) receptor level was significantly higher in the CON and AEX groups than in the ACON group (p<0.01). TUNEL assay showed a significant reduction in apoptosis in the AEX group (p<0.001). Caspase-3 activation was significantly decreased in the AEX and CON groups (p<0.05). These results show that forced moderate-intensity treadmill exercise increases the level of NGF and activates P-PI3-K to induce P-Akt in order to suppress apoptotic cell death in the hippocampus of induced aging rats.
Authors:
Chang-Hun Chae; Hyun-Tae Kim
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-14
Journal Detail:
Title:  Neurochemistry international     Volume:  55     ISSN:  1872-9754     ISO Abbreviation:  Neurochem. Int.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-06-15     Completed Date:  2009-09-02     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8006959     Medline TA:  Neurochem Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  208-13     Citation Subset:  IM    
Affiliation:
School of Sport Science, Sungkyunkwan University, Chunchun-dong, Jangan-gu, Suwon 440-746, South Korea.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / metabolism*
Aging / drug effects,  metabolism*
Animals
Apoptosis / physiology*
Cognition Disorders / drug therapy,  metabolism,  physiopathology
Exercise Test
Exercise Therapy / methods
Galactose / pharmacology
Hippocampus / metabolism*,  physiopathology
Male
Memory Disorders / metabolism,  physiopathology,  therapy
Nerve Degeneration / metabolism,  physiopathology,  therapy
Nerve Growth Factor / metabolism*
Phosphorylation
Physical Conditioning, Animal / physiology*
Proto-Oncogene Proteins c-akt / metabolism
Rats
Rats, Sprague-Dawley
Signal Transduction / physiology
Up-Regulation / drug effects,  physiology
Chemical
Reg. No./Substance:
26566-61-0/Galactose; 9061-61-4/Nerve Growth Factor; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt

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


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