Neurochem Int. 2010 Jan;56(2):203-4; author reply 205-7. doi: 10.1016/j.neuint.2009.07.013.
Vasogenic mechanism of brain edema in acute liver failure (ALF) remains poorly understood. Recent work demonstrates that matrix metalloproteinase-9 (MMP-9) contributes to the development of brain edema in experimental ALF (J Hepatol 44:1105, 2006). Importantly, MMP-9 blockage with specific monoclonal antibodies and/or synthetic inhibitor, the edema is attenuated. Specifically, utrastructural evaluations demonstrate intact blood-brain barrier and its tight junction. These results suggest that subtle alterations in BBB are likely to involve in the brain edema associated with ALF.
血管源性脑水肿在急性肝衰竭（ALF）中的发病机制尚不清楚。最近的研究表明，基质金属蛋白酶-9（MMP-9）参与了实验性 ALF 中脑水肿的形成（J Hepatol 44:1105, 2006）。重要的是，用特异性单克隆抗体和/或合成抑制剂阻断 MMP-9，脑水肿会减轻。具体而言，超微结构评估显示血脑屏障及其紧密连接完整。这些结果表明，与 ALF 相关的脑水肿可能与 BBB 的细微改变有关。
