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|a pubmed25n0658.xml
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|a (DE-627)NLM197409458
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|a (NLM)20398468
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a chi
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| 100 |
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|a Zhao, Ya-ning
|e verfasserin
|4 aut
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|a Effect of edaravone on extracellular signal-regulated kinase 1/2 pathway following severe traumatic brain injury in rats
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|c 2010
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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| 338 |
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|a Band
|b nc
|2 rdacarrier
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| 500 |
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|a Date Completed 08.07.2011
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|a Date Revised 01.12.2018
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|a published: Print
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|a Citation Status MEDLINE
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|a OBJECTIVE: To study the protective effect of edaravone on severe traumatic brain injury (TBI) and its potential mechanism
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|a METHODS: Two hundred and seventy-three male Sprague-Dawley (SD) rats were divided randomly into four groups: control group (n=45), model group (n=88), low-dose edaravone treatment group (n=72), high-dose edaravone treatment group (n=68). TBI rat model was reproduced by weight-dropping injury. One, 6, 24, 48 and 72 hours after injury, changes in brain tissue were observed with light and electron microscopy. The expression of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) was determined by Western blotting. The rate of neuron apoptosis was observed with immunohistochemistry and terminal-deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method. Learning and memory function assessments were performed with Morris water maze from 7th day to 10th day after injury
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|a RESULTS: Compared with control group, a part of neurons in hippocampus displayed histopathologic changes denoting necrosis 6, 24, 48 and 72 hours after injury. The p-ERK1/2 expression level (pg/unit) increased 1, 6, 24, 48 hours after injury (2.05 + or - 0.40, 4.40 + or - 0.96, 6.70 + or - 0.87, 3.67 + or - 0.28 vs. 0.40 + or - 0.04, 0.41 + or - 0.05, 0.43 + or - 0.06, 0.40 + or - 0.03), and the number of apoptotic cells increased 6, 24, 48, 72 hours after injury (9.60 + or - 2.69, 12.68 + or - 2.99, 16.94 + or - 3.92, 25.82 + or - 4.61 vs. 2.42 + or - 0.38, 2.58 + or - 0.57, 2.74 + or - 0.56, 2.61 + or - 0.58); latent period to find the safety platform (s) was significantly prolonged (119.8 + or - 25.0, 105.6 + or - 24.5, 98.5 + or - 21.8, 92.0 + or - 19.5 vs. 49.5 + or - 7.5, 32.7 + or - 6.3, 25.8 + or - 6.5, 24.8 + or - 5.5, all P<0.05). After treatment with edaravone, the degree of morphological injury, p-ERK1/2 level and number of apoptotic neurons decreased, latent period to find the safety platform was significantly shortened (in low-dose edaravone treatment group, p-ERK1/2 expression level at 6, 24, 48 hours was 2.46 + or - 0.22, 4.00 + or - 0.84, 2.38 + or - 0.32, and in high-dose edaravone treatment group was 1.67 + or - 0.15, 1.86 + or - 0.38, 1.27 + or - 0.28; in low-dose edaravone treatment group, the apoptotic cells at 6, 24, 48, 72 hours was 5.20 + or - 1.23, 7.10 + or - 1.72, 9.54 + or - 1.36, 14.12 + or - 3.19, and in high-dose edaravone treatment group was 3.40 + or - 0.49 , 4.39 + or - 0.73, 5.02 + or - 1.12, 8.78 + or - 2.16; in low-dose edaravone treatment group, latent period to find the safety platform at 7-10 days was 94.8 + or - 22.8, 65.2 + or - 19.0, 62.0 + or - 16.7, 59.5 + or - 15.6, and in high-dose edaravone treatment group it was 81.5 + or - 20.7, 55.4 + or - 18.5, 40.0 + or - 12.3, 32.2 + or - 11.0, all P<0.05). High-dose edaravone showed a better effect (all P<0.05)
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|a CONCLUSION: Edaravone gives good therapeutic effect on severe TBI, and the molecular mechanism is related to attenuation of ERK1/2 pathway and neuronal apoptosis following severe brain trauma
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Mitogen-Activated Protein Kinase 1
|2 NLM
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| 650 |
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|a EC 2.7.11.24
|2 NLM
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| 650 |
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|a Mitogen-Activated Protein Kinase 3
|2 NLM
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| 650 |
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|a EC 2.7.11.24
|2 NLM
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| 650 |
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|a Edaravone
|2 NLM
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| 650 |
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|a S798V6YJRP
|2 NLM
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| 650 |
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|a Antipyrine
|2 NLM
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| 650 |
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|a T3CHA1B51H
|2 NLM
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| 700 |
1 |
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|a Guo, Xia
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Gao, Jun-ling
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Chen, Hai-hong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Tian, Yan-xia
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Cui, Jian-zhong
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
|d 1998
|g 22(2010), 4 vom: 19. Apr., Seite 230-3
|w (DE-627)NLM098227793
|x 1003-0603
|7 nnns
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| 773 |
1 |
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|g volume:22
|g year:2010
|g number:4
|g day:19
|g month:04
|g pages:230-3
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|a AR
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|d 22
|j 2010
|e 4
|b 19
|c 04
|h 230-3
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