Literature DB >> 23515469

Effective protection of rabbits' explosive brain injury through blocking gap junction communication.

Z Yong-Ming1, L Jia-Chuan, Y Yan-Yan, S Wen-Jiang, T Hong, L Bing-Cang, Z Liang-Chao.   

Abstract

BACKGROUND: The gap junction plays an important role in spreading of apoptotic and necrotic signals from injured and stressed cells to the neighboring viable cells. The present study was performed to investigate the important role of gap junction communication on rabbits' explosive brain injury.
METHODS: Explosion of paper detonators was used to create explosive brain injury model in 60 rabbits, which was randomly divided into control group and experimental group. Octanol, an efficient blocker of gap junction, was injected in the left ventricle to block gap junction communication in the experimental group 2 hours before injury, while the same volume of saline was utilized in the control group.
RESULTS: Penumbra volume around the brain contusion in the experimental group was significantly less than that in the control group at 1d and 3d after brain damage. RT-PCR and Western blotting analysis indicated that the expression of connexin-43 (Cx43) and caspase-3 was significantly lower in the experimental group than that in the control group at all time points.
CONCLUSION: Rabbits' explosive brain injury can be efficiently attenuated through blocking the gap junction communication, which benefit for deeper understanding the mechanism of brain injury.

Entities:  

Keywords:  caspase-3; connexin-43 (Cx43); explosive brain injury

Mesh:

Substances:

Year:  2012        PMID: 23515469      PMCID: PMC3598299          DOI: 10.4314/ahs.v12i4.24

Source DB:  PubMed          Journal:  Afr Health Sci        ISSN: 1680-6905            Impact factor:   0.927


  13 in total

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Authors:  N Homma; J L Alvarado; W Coombs; K Stergiopoulos; S M Taffet; A F Lau; M Delmar
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2.  Acute death of astrocytes in blast-exposed rat organotypic hippocampal slice cultures.

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Review 3.  Relevance of gap junctions and large pore channels in traumatic brain injury.

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4.  Hypoxia preconditioning protects neuronal cells against traumatic brain injury through stimulation of glucose transport mediated by HIF-1α/GLUTs signaling pathway in rat.

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