Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema

作     者：Wanyin Ren Guojie Jing Qin Shen Xiaoteng Yao Yingchao Jing Feng Lin Weidong Pan 

作者机构：Guangdong Medical College Huizhou First People's Hospital 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2013年第8卷第29期

页      面：2703-2712页

核心收录：

学科分类：1002[医学-临床医学] 100210[医学-外科学(含：普外、骨外、泌尿外、胸心外、神外、整形、烧伤、野战外)] 10[医学] 

基　　金：supported by the Natural Science Foundation of Guangdong Province No.10151600101000002 

主　　题：neural regeneration traumatic brain injury brain edema connexin 43 occludin nerve cells pa-thology tight junction grants-supported paper neuroregeneration 

摘      要：The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney＇s free falling method. The brains were harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury. Changes in brain water content were determined using the wet and dry weights. Our results showed that water content of tissue significantly increased after traumatic brain injury, and reached minimum at 24 hours. Hematoxylin-eosin staining revealed pathological impairment of brain tissue at each time point after injury, particularly at 3 days, with nerve cell edema, degenera- tion, and necrosis observed, and the apoptotic rate significantly increased. Immunohistochemistry and western blot analysis revealed that the expression of occludin at the injured site gradually de- creased as injury time advanced and reached a minimum at 3 days after injury; the expression of connexin 43 gradually increased as injury time advanced and reached a peak at 24 hours after in-jury. The experimental findings indicate that changes in occludin and connexin 43 expression were consistent with the development of brain edema, and may reflect the pathogenesis of brain injury.