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Brain‐derived Neurotrophic Factor Mediates the Neuro‐protective Effects of Estrone after Brain Injury
Author(s) -
Gatson Joshua W.,
Simpkins James,
Wigginton Jane,
Liu Ming-Mei,
Wolf Steven,
Minei Joseph
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.672.2
Subject(s) - estrone , creb , neurotrophic factors , traumatic brain injury , endocrinology , medicine , brain derived neurotrophic factor , brain damage , estrogen , chemistry , biochemistry , receptor , psychiatry , transcription factor , gene
Estrone (predominant estrogen in postmenopausal women) has shown to be a promising neuro‐protective agent in stroke and other traumatic injuries. The overall goal of this project was to determine if ERK signaling and brain‐derived neurotrophic factor (BDNF) mediates the protective effects of estrone after TBI. Methods In this study, male rats were treated with either placebo (corn oil; n=8) or estrone (0.5mg/kg; n=8) at 30 minutes after TBI. Injury was induced using the controlled cortical impact device. Control (n=8) and sham (craniotomy only; n=8) groups were also included in this study. At 72 hours following injury, the brains were fixed and stained for TUNEL + cells. To test for phospho‐ ERK, phospho‐CREB, and BDNF levels, total protein was isolated from brain tissue and Western analysis was used. Results Estrone significantly decreased the levels of TUNEL + staining (p<0.01). In addition, in the estrone treated groups there was a significant increase in the levels of phospho‐ERK (p<0.02) and CREB (p<0.05). Also, the levels of BDNF (p<0.007) were significantly increased in the estrone treated groups at 72 hours after injury. Conclusion Estrone given after injury is protective and results in an increase in ERK signaling and subsequent BDNF expression. These results suggest that other estrogens in addition to estradiol may afford individuals protection from secondary brain injury after TBI.