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血管源性脑水肿 (VBE)是脑缺血病例急性期死亡的主要原因 ,研究其分子生物学机制对有效地预防与治疗VBE具有重要意义。基质金属蛋白酶 (MMP ,主要是MMP 9)与脑缺血后ECM降解和血脑屏障 (BBB)通透性增加密切相关。正常时MMPs内源性抑制剂 (TIMPs)与MMPs保持相对平衡。脑缺血后早期应用MMP抑制剂可阻断或减轻VBE。
Vascular brain edema (VBE) is the main cause of death in the acute phase of cerebral ischemia. To study its molecular biological mechanism is of great significance for the effective prevention and treatment of VBE. Matrix metalloproteinases (MMPs, mainly MMPs 9) are closely related to the degradation of ECMs and the increased permeability of the blood-brain barrier (BBB) after cerebral ischemia. Normal MMPs endogenous inhibitors (TIMPs) and MMPs remain relatively balanced. Early application of MMP inhibitors after cerebral ischemia can block or reduce VBE.