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血脑屏障的破坏是引起脑缺血损伤及继发水肿、出血、炎症的微观原因。缺血缺氧和再灌注过程产生的自由基,以及后续基质金属蛋白酶的激活,是破坏血脑屏障结构和功能的重要分子机制。因而,在脑缺血早期及时抑制自由基产生并清除自由基,抑制基质金属蛋白酶的活性,是降低脑缺血血脑屏障损伤及其并发症的关键环节。本文将从血脑屏障损伤的角度,概述自由基与基质金属蛋白酶在脑缺血损伤过程中的作用。
The destruction of the blood-brain barrier is the microscopic cause of cerebral ischemia and secondary edema, hemorrhage and inflammation. Free radicals produced during ischemia, hypoxia and reperfusion, as well as the subsequent activation of matrix metalloproteinases, are important molecular mechanisms that undermine the structure and function of the blood-brain barrier. Therefore, in the early stage of cerebral ischemia in a timely manner to inhibit the generation of free radicals and scavenging free radicals, inhibition of the activity of matrix metalloproteinase, is to reduce cerebral blood flow in the brain barrier damage and complications of the key link. This article will outline the role of free radicals and matrix metalloproteinases in the process of cerebral ischemic injury from the perspective of blood-brain barrier injury.