Regulation of aquaporin-4 in a traumatic brain injury model in rats
Regulation of aquaporin-4 in a traumatic brain injury model in rats
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DOI：
10.3171/jns.2003.98.3.0565
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发表时间：
2003-03-01
影响因子：
4.1
通讯作者：
Tsui, JKC
中科院分区：
文献类型：
--
作者：
Sun, MC;Honey, CR;Tsui, JKC
目的。水通道蛋白-4 (AQP4) 在调节脑水稳态中发挥着重要作用。在这项研究中，作者研究了大鼠局灶性皮质挫伤后 AQP4 的调节。方法。三十三只成年雄性 Wistar 大鼠的顶叶皮质受到局灶性皮质挫伤。另外九只大鼠接受了颅骨切除术，但没有造成任何创伤（假伤）。 1、4和24小时后处死动物。通过比较每个半球的湿重和干重来检查大鼠大脑的含水量。通过逆转录聚合酶链式反应测量 Aquaporin-4 信使 (m)RNA。计算每只动物损伤部位（顶叶皮层）、邻近部位（枕叶皮质）和远离损伤部位（额极皮层）受损半球与对侧对照半球的 AQP4 mRNA 表达比率。损伤部位脑水肿明显增加。 AQP4 mRNA的表达在损伤部位显着升高，邻近损伤部位显着降低，而在远离损伤部位则无显着差异。受损顶叶皮质的 AQP4 mRNA 上调程度与邻近枕叶皮质的下调程度相关。结论。这项研究的数据表明，AQP4 的上调发生在创伤性脑损伤部位，而该分子的下调发生在损伤部位附近。了解 AQP4 的生理学及其在脑损伤后的调节可能有助于开发治疗头部损伤引起的脑水肿的新疗法。
Object. Aquaporin-4 (AQP4) plays a significant role in the regulation of brain water homeostasis. In this study the authors investigated the regulation of AQP4 following a focal cortical contusion injury in rats.Methods. Thirty-three adult male Wistar rats received a focal cortical contusion of the parietal cortex. An additional nine rats underwent a craniectomy, but no trauma was inflicted (sham injury). Animals were killed 1, 4, and 24 hours later. The rat brains were examined for water content by comparing the wet and dry weights of each hemisphere. Aquaporin-4 messenger (m)RNA was measured by reverse transcription-polymerase chain reaction. A ratio of AQP4 mRNA expression in the lesioned hemisphere compared with that in the contralateral control hemisphere was calculated for each animal at the injury site (parietal cortex) and at sites adjacent to (occipital cortex) and distant from the injury (frontal pole cortex).Brain edema was significantly increased at the injury site. The expression of AQP4 mRNA was significantly increased at the injury site, significantly decreased adjacent to the injury site, and not significantly different at a site distant from the injury. The magnitude of AQP4 mRNA upregulation at the injured parietal cortex correlated with the degree of downregulation in the adjacent occipital cortex.Conclusions. Data from this study demonstrate that an upregulation of AQP4 occurs at the site of traumatic brain injury and that a downregulation of this molecule occurs adjacent to the site of injury. Understanding the physiology of AQP4 and its regulation following brain injury may allow for the development of novel treatments for cerebral edema that accompanies head injury.