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大鼠胎鼠显性脊柱裂与 c-Jun N-末端激酶信号的相关性。

Correlation between spina bifida manifesta in fetal rats and c-Jun N-terminal kinase signaling.

机构信息

Department of Cancer, the 463 Hospital of Chinese PLA, Shenyang 110042, Liaoning Province, China ; Division of Health, Bureau of Guard, General Advisor Office of Chinese PLA, Beijing 100017, China.

Medical Department, the 463 Hospital of Chinese PLA, Shenyang 110042, Liaoning Province, China.

出版信息

Neural Regen Res. 2012 Nov 15;7(32):2485-91. doi: 10.3969/j.issn.1673-5374.2012.32.001.

DOI:10.3969/j.issn.1673-5374.2012.32.001
PMID:25337099
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4200703/
Abstract

Fetal rat models with neural tube defects were established by injection with retinoic acid at 10 days after conception. The immunofluorescence assay and western blot analysis showed that the number of caspase-3 positive cells in myeloid tissues for spina bifida manifesta was increased. There was also increased phosphorylation of c-Jun N-terminal kinase, a member of the mitogen activated protein kinase family. The c-Jun N-terminal kinase phosphorylation level was positively correlated with caspase-3 expression in myeloid tissues for spina bifida manifesta. Experimental findings indicate that abnormal apoptosis is involved in retinoic acid-induced dominant spina bifida formation in fetal rats, and may be associated with the c-Jun N-terminal kinase signal transduction pathway.

摘要

采用维甲酸在受孕后 10 天对胎鼠模型进行注射,建立神经管缺陷胎鼠模型。免疫荧光检测和 Western blot 分析显示,显性脊柱裂髓质组织中 caspase-3 阳性细胞的数量增加。丝裂原活化蛋白激酶家族成员 c-Jun N 末端激酶的磷酸化也增加。显性脊柱裂髓质组织中 c-Jun N 末端激酶的磷酸化水平与 caspase-3 的表达呈正相关。实验结果表明,异常细胞凋亡参与了维甲酸诱导的胎鼠显性脊柱裂的形成,可能与 c-Jun N 末端激酶信号转导通路有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/f5a5b68e1ea3/NRR-7-2485-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/4eb5ed24a03b/NRR-7-2485-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/21b2f6ba86be/NRR-7-2485-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/4df2b5c8e093/NRR-7-2485-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/f5a5b68e1ea3/NRR-7-2485-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/4eb5ed24a03b/NRR-7-2485-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/21b2f6ba86be/NRR-7-2485-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/4df2b5c8e093/NRR-7-2485-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/4200703/f5a5b68e1ea3/NRR-7-2485-g005.jpg

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本文引用的文献

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WITHDRAWN: Periconceptional supplementation with folate and/or multivitamins for preventing neural tube defects.撤回:孕前补充叶酸和/或多种维生素预防神经管缺陷。
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Ethanol induces mouse spermatogenic cell apoptosis in vivo through over-expression of Fas/Fas-L, p53, and caspase-3 along with cytochrome c translocation and glutathione depletion.乙醇通过 Fas/Fas-L、p53 和 caspase-3 的过表达以及细胞色素 c 易位和谷胱甘肽耗竭诱导体内小鼠生精细胞凋亡。
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Down-regulation of telomerase activity and activation of caspase-3 are responsible for Tanshinone I-induced apoptosis in monocyte leukemia cells in vitro.端粒酶活性下调和半胱天冬酶-3激活是丹参酮I体外诱导单核细胞白血病细胞凋亡的原因。
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