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脑梗死后继发的炎症反应影响脑梗死的进展和转归，抑制脑梗死后炎症反应对实验性卒中具有治疗作用。因此，通过抑制炎症反应有望为减轻脑梗死损伤提供一种有效的治疗措施。脑梗死后激肽释放酶-激肽系统( KKS)激活，可减轻脑梗死后炎症反应，促进神经功能修复。转染激肽释放酶基因可促进胶质细胞存活和迁移，抑制氧化应激产物生成，从而减轻脑梗死后神经功能缺损。研究脑梗死后KKS对机体炎症反应的调控机制有助于指导脑梗死的治疗。“,”Secondary inflammatory response is now considered to contribute to the progression and prog-nosis after cerebral infarction. Inhibition of inflammation has shown protective effect on experimental stroke. Thus,antiinflammation may provide an effective intervertion to reduce cerebral ischemic injuries. Studies have shown that the activation of the kallikrein-kinin system( KKS) after cerebral infarction may suppress cerebral inflammation,and improve the neurological recovery. Kallikrein gene transfer provides neuroprotection against Cerebral infarction by enhancing glial cell survival and migration and reducing cerebral superoxide produc-tion. Further elucidation on the regulatory mechanisms of KKS in the inflammation will be beneficial to the treatment of cerebral ischemia.