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231223s2007 xx ||||| 00| ||chi c |
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|a pubmed25n0566.xml
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|a (DE-627)NLM169873153
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|a (NLM)17456344
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a chi
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| 100 |
1 |
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|a Chen, Jian
|e verfasserin
|4 aut
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| 245 |
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|a Acanthopanax Senticosus Saponins induced tolerance to ischemia and its possible molecular mechanism in PC12 cells
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|c 2007
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| 336 |
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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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|a Date Completed 03.06.2010
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|a Date Revised 07.06.2016
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|a published: Print
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|a Citation Status MEDLINE
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|a OBJECTIVE: To study the tolerance to ischemia induced by Acanthopanax Senticosus Saponins (ASE) in PC12 cells and the involved mechanism
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|a METHODS: An ischemic model was developed in PC12 cell line by treatment with oxygen-glucose deprivation. The effects of ASE pretreatment on tolerance of PC12 cells to ischemia were evaluated by MTT assay and analysis of cellular morphology. The expression of hypoxia-inducing factor (HIF)-1alpha, erythropoietin (EPO) after the pretreatment with ASE was detected by Western blotting. The DNA binding activities of HIF-1 in PC12 cells with the pretreatment of ASE were demonstrated by using electrophoretic mobility shift assay (EMSA)
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|a RESULTS: In ischemia model, the viability of PC12 cells was decreased to (49.12 +/- 3.22)% after oxygen-glucose deprivation for 9 hours. However, ASE (50 microg/ml) pretreatment could remarkably increase the viability of PC12 cells by (67.97 +/- 2.92)%. There were significant differences between the experimental group and control group (F = 473.67, P < 0.01). The cellular morphology showed that PC12 cells exposed for 7 days to nerve growth factor (NGF) exhibited round, smooth cell bodies with normal processes and that processes formed extensive network. At 9 hour after ischemia, cell bodies of many PC12 cells were found shrinken, the processes were disrupted and network disappeared. However, pretreatment with ASE (50 microg/ml) could largely prevent the morphological damage to PC12 cells that would have caused by subsequent exposure to 9 h ischemic insult, many cellular bodies were intact and many processes and network of PC12 cells still existed. The expression of HIF-1alpha increased after pretreatment with ASE shown by Western blot. There were significant differences between the experimental group and control group (F = 167.18, P < 0.01). The DNA binding activities of HIF-1 in PC12 cells after pretreatment with ASE was significantly increased, and it could activate the expression of EPO (F = 128.37, P < 0.01)
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|a CONCLUSIONS: The pretreatment with ASE could induce tolerance against ischemia in PC12 cells. The elevated expression and increased DNA binding activity of HIF-1alpha, the overexpression of its downstream target EPO may be the molecular mechanism in tolerance of PC12 cells to ischemia induced by ASE pretreatment
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|a English Abstract
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|a Journal Article
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|a Hypoxia-Inducible Factor 1, alpha Subunit
|2 NLM
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| 650 |
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|a Saponins
|2 NLM
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| 650 |
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|a Erythropoietin
|2 NLM
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| 650 |
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|a 11096-26-7
|2 NLM
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| 700 |
1 |
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|a Zhu, Li
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Pan, Yong-jin
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Zhonghua er ke za zhi = Chinese journal of pediatrics
|d 1960
|g 45(2007), 2 vom: 25. Feb., Seite 138-42
|w (DE-627)NLM136249191
|x 0578-1310
|7 nnns
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| 773 |
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|g volume:45
|g year:2007
|g number:2
|g day:25
|g month:02
|g pages:138-42
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