Department of Infectious Diseases, The First Affiliated Hospital, China Medical University, Shenyang 110001, China.
Gastroenterol Res Pract. 2013;2013:841707. doi: 10.1155/2013/841707. Epub 2013 May 26.
Brain edema in acute liver failure (ALF) remains lethal. Cytotoxic mechanisms associated with brain edema have been well recognized, but the role of vasogenic mechanisms of brain edema has not been explored. Intact tight junctions (TJs) between brain capillary endothelial cells are critical for normal BBB function. Recent reports found significant alterations in the tight junction elements including occludin and claudin-5, suggesting a vasogenic injury in the blood-brain barrier (BBB) integrity. However, the role of TJ in ALF has not been completely understood. This paper reviews the role of the paracellular tight junction in the increased selective BBB permeability that leads to brain edema in ALF and furthermore explores the effect of systemic inflammatory cytokines on the tight junction dysfunction.
急性肝衰竭（ALF）中的脑水肿仍然是致命的。与脑水肿相关的细胞毒性机制已得到充分认识，但血管源性脑水肿机制的作用尚未得到探索。脑毛细血管内皮细胞之间完整的紧密连接（TJ）对于正常的 BBB 功能至关重要。最近的报道发现，紧密连接元件（包括紧密连接蛋白和 Claudin-5）发生了明显改变，提示血脑屏障（BBB）完整性存在血管源性损伤。然而，TJ 在 ALF 中的作用尚未完全阐明。本文综述了细胞旁紧密连接在增加选择性 BBB 通透性导致 ALF 脑水肿中的作用，并进一步探讨了全身炎症细胞因子对紧密连接功能障碍的影响。
