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Occludin and connexin 43 expression in the pathogenesis of traumatic brain edema

November 27th, 2013
Occludin and connexin 43 expression in the pathogenesis of traumatic brain edema
Expression of connexin 43 in the brain of rats at 24 hours after traumatic brain injury (immunohistochemical staining, × 400). Credit: Neural Regeneration Research

Understanding the pathogenesis of brain edema may allow for the prevention and treatment of edema in the field of neurosurgery, thus resulting in better treatments for intracranial diseases.

Wanyin Ren and colleagues from Guangdong Medical College, China established an experimental model of traumatic brain injury in Sprague-Dawley rats according to Feeney's free falling method, and harvested the brains harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury for observing pathological changes of brain tissues and expression of occludin and connexin 43. They found that changes in occludin and connexin 43 expression were consistent with the development of brain edema, and may reflect the pathogenesis of brain injury. These findings were published in the Neural Regeneration Research (Vol. 8, No. 29, 2013).

More information:
Ren WY, Jing GJ, Shen Q, Yao XT, Jing YC, Lin F, Pan WD. Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema. Neural Regen Res. 2013;8(29):2703-2712.

Provided by Neural Regeneration Research

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