高压氧对急性一氧化碳中毒大鼠少突胶质细胞前体细胞ADAM10 mRNA表达的影响

Abstract
Figure/Table
References (21)
Related Citation (2)

Download: PDF (556 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the effect of hyperbaric oxygen （HBO) treatment on the xpression of Oligodendrocyte Precursors （OPCs) ADAM10 mRNA in the acute carbon monoxide poisoning（ACOP) rats. Methods OPCs cells of neonatal rat were cultured in vitro and divided into three groups: control, ACOP and HBO groups. Control group: no treatment, ACOP group: the OPC cells were placed in a sealed container and injected with 1% carbon monoxide according to the volume ratio, HBO group: OPCs cells after ACOP were placed in animal experiments of hyperbaric oxygen chamber, with 98% O2, 2%CO2 washing 10 min, then 15 min 0.35 MPa pressure staying 2 h, at last 20 min reducing to normal pressure. The chamber temperature was controlled at 37℃. The end time of HBO treatment was set as 0 h, the three groups were collected at 6 , 24 h and 48 h for subsequent experiments. The expression of ADAM10 mRNA at 6, 24 h, and 48 h were detected by RT-PCR. Results 6, 24 h, and 48 h, the expression of ADAM10 mRNA was no change in control group, but gradually decreased in ACOP group, and increased in HBO group, there was statistically significant among the three groups (F = 8.491, P < 0.01). Compared with control group, the expression of ADAM10 mRNA at 6, 24, 48 h was significantly reduced in ACOP group, while was significantly increased in HBO group （F = 88.692, P < 0.01). Conclusion ADAM10 of OPCs may play an important role in the injury of central nervous system after ACOP and HBO.

Key words： Hyperbaric Oxygen acute carbon monoxide poisoning Oligodendrocyte precursors ADAM10

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	GUO Dazhi FENG Yuan HU Huijun LI Na PAN Shuyi

Cite this article:

GUO Dazhi FENG Yuan HU Huijun LI Na PAN Shuyi. Hyperbaric oxygen on the expression of ADAM10 of rat oligodendrocyte precursors in vitro after acute carbon monoxide poisoning[J]. 中国医药导报, 2018, 15(5): 9-12.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2018/V15/I5/9

[1] Wu PE，DN Juurlink. Carbon monoxide poisoning [J]. Cmaj，2014，186（8）：611.
[2] 武涛，杨小军，党根喜，等.一氧化碳中毒迟发性脑病临床和MRI研究[J].中国实用神经疾病杂志，2010，13（15）：10-12.
[3] Edwards DR，Handsley MM，Pennington CJ. The ADAM metalloproteinases [J]. Mol Aspects Med，2008，29（5）：258-89.
[4] Jangouk P，Dehmel T，Meyer Zu H?rste G，et al. Involvement of ADAM-10 in axonal outgrowth and myelination of the peripheral nerve [J]. Glia，2009，57（16）：1765-1774.
[5] Yang YJ，Wang XL，Yu XH，et al. Hyperbaric oxygen induces endogenous neural stem cells to proliferate and differentiate in hypoxic-ischemic brain damage in neonatal rats [J]. Undersea Hyperb Med，2008，35（2）：113-129.
[6] Thom SR，Bhopale VM，Fisher D. Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity [J]. Toxicol Appl Pharmacol，2006，213（2）：152-159.
[7] 郭大志，冯园，胡慧军，等.急性一氧化碳中毒对大鼠大脑少突胶质细胞前体细胞分化功能的影响[J].中华航海医学与高气压医学杂志，2017，24（3）：200-204.
[8] Lopez Juarez A，He D，Richard Lu Q. Oligodendrocyte progenitor programming and reprogramming：Toward myelin regeneration [J]. Brain Res，2016，1638（Pt B）：209-220.
[9] Saftig P，Lichtenthaler SF. The alpha secretase ADAM10：A metalloprotease with multiple functions in the brain [J]. Prog Neurobiol，2015，135：1-20.
[10] Bernstein HG，Bukowska A，Krell D，et al. Comparative localization of ADAMs 10 and 15 in human cerebral cortex normal aging，Alzheimer disease and Down syndrome [J]. J Neurocytol，2003，32：153-160.
[11] Kieseier BC，Pischel H，Neuen-Jacob E，et al. ADAM-10 and ADAM-17 in the inflamed human CNS [J]. Glia，2003， 42（4）：398-405.
[12] Hartmann D，de Strooper B，Serneels L，et al. The disintegrin/metalloprotease ADAM 10 is essential for Notch signalling but not for alpha-secretase activity in fibroblasts [J]. Hum Mol Genet，2002，11（21）：2615-2624.
[13] Schimmelpfeng K，Gögel S，Klämbt C. The function of leak and kuzbanian during growth cone and cell migration [J]. Mech Dev，2001，106（1-2）：25-36.
[14] Thom SR，Bhopale VM，Fisher D，et al. Delayed neuropathology after carbon monoxide poisoning is immune-mediated [J]. Proc Natl Acad Sci U S A，2004，101（37）：13 660-13 665.
[15] 孙瑞佼，郭大志，李航，等.急性一氧化碳中毒对大鼠少突胶质前体细胞的影响[J].中国康复，2015，30（1）：10-13.
[16] Wang WL，Chang YM，Jinsheng L. Expressions of the astrocytes and oligodendrocytes in rat models of delayed neuropathological sequelaeaer CO poisoning and the efect of hyperbaric oxygen treatment on the two kinds of neuroglia cell [J]. China Crit Care Med，2007，27：615-618.
[17] 郭大志，冯园，沈晨，等.一氧化碳中毒对大鼠少突胶质细胞前体细胞迁移的影响[J].中国医药导报，2016，13（36）：49-52.
[18] 李温仁，倪国坛.高压氧医学[M].上海科学技术出版社，1998：476-478.
[19] Weaver LK，Hopkins RO，Chan KJ，et al. Hyperbaric oxygenfor acute carbon monoxide poisoning [J]. N Engl J Med，2002，347（14）：1057-1067.
[20] 乔坤，谢小梅，涂超群，等.高压氧对急性一氧化碳中毒的治疗[J].中华急诊医学杂志，2006，15（7）：662-663.
[21] Juri■ DM，Šuput D，Brvar M. Hyperbaric oxygen preserves neurotrophic activity of carbon monoxide-exposed astrocytes [J]. Toxicol Lett，2016，253：1-6.