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癫反复发作的机制一直未完全明了,当前的研究表明癫的反复发作,导致血脑屏障破坏,随后外周血中白蛋白进入中枢,但其在脑脊液中的浓度难以检测。进入中枢的白蛋白通过依赖转化生长因子-β(TGF-β)信号通路导致钾内向整流通道和水通道蛋白4下调,诱导和维持中枢的神经炎症,影响缝隙连接偶联,参与兴奋性递质转运;以及通过非依赖TGF-β信号通路上调基质金属蛋白酶-9,降低扩散性去极化,导致神经元死亡,缓冲抗癫药物浓度等影响脑的兴奋性,促进癫的反复发作。而针对相关机制的干预研究也提供了抗新思路。
The mechanism of recurrent epilepsy has not been completely understood. Current studies show that recurrent epilepsy, leading to the destruction of the blood-brain barrier, followed by albumin into the central peripheral blood, but its concentration in cerebrospinal fluid is difficult to detect. Into the central albumin relies on the transforming growth factor-β (TGF-β) signaling pathway leading to potassium inward rectifier channels and aquaporin 4 downregulation, inducing and maintaining central neuroinflammation, affecting gap junctional coupling, participation in excitatory neurotransmitters Translocation; and through the TGF-β signaling pathway upregulation of matrix metalloproteinase-9, to reduce the proliferation of depolarization, leading to neuronal death, buffer the concentration of anti-epileptic drugs affect the excitability of the brain and promote the recurrent seizures. Intervention studies on related mechanisms also provide a new anti-思 idea.