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在脑缺血损伤机制中,基质金属蛋白酶(MMPs)及其内源性抑制剂(TIMPs)的作用日益受到重视。研究表明,TIMP-3、MMP-3及其复合体介导了多种细胞生理和病理发生、发展机制;它们参与了脑缺血再灌注损伤后炎性级联反应及细胞凋亡等机制;同时也参与动脉粥样硬化斑块形成与破裂等。通过研究TIMP-3、MMP-3与脑缺血再灌注损伤的相关性,将有利于脑缺血后神经保护治疗及预防脑缺血发生。
In the mechanism of cerebral ischemia injury, the role of matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) is gaining more and more attention. Studies have shown that TIMP-3, MMP-3 and their complexes mediate a variety of cell physiological and pathological mechanisms of development and progression; they are involved in mechanisms such as inflammatory cascade and apoptosis after cerebral ischemia-reperfusion injury; Also involved in atherosclerotic plaque formation and rupture. By studying the relationship between TIMP-3, MMP-3 and cerebral ischemia-reperfusion injury, it is good for neuroprotective therapy and prevention of cerebral ischemia after cerebral ischemia.