张天宇， 刘月阳， 袁琳琳， 杨静玉^*

（  沈阳药科大学药理系，沈阳 110016；  ）

摘要： 缺血性脑卒中的致死率和致残率极高，严重威胁着患者生命与生存质量，其复杂的病理生理过程可在短时间内引发广泛的缺血性细胞死亡。多种机制参与这一过程，而其中钙离子超载在这一损伤过程中占据重要地位。研究认为，脑缺血发生后，经由N-甲基-D-天冬氨酸受体 (N-methyl-D-aspartic acid receptor, NMDAR) 持续活化介导的胞外钙离子内流，以及内质网ATP酶2 (Sarcoplasmic/endoplasmic reticulum ATPase 2, SERCA2) 损伤造成的内质网应激 (Endoplasmic reticulum stress, ERS) 引发的内源性钙库释放，是造成胞内钙离子超载的主要原因。因此，及时恢复细胞内钙稳态，成为治疗缺血性脑卒中的重要环节之一。
关键词： 药理学;缺血性脑中风;钙超载

ZHANG tianyu， LIU yueyang， YUAN linlin， YANG jingyu^*

（  Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang 110016；  ）

Abstract： Stroke is one of the major contributors of mortality and morbidity worldwide. It results due to sudden blockade of blood flw into the brain thereby leading to a wide range of ischemic cell death in a short time. Cell death following cerebral ischemia is a result of complex pathophysiological mechanisms involving various cellular components, and calcium is one of the key factors that exacerbate the injury process. It is also known that, excessive calcium inflx through over-stimulated N-methyl-D-aspartate receptor (NMDAR), as well as release from endoplasmic reticulum in the case of endoplasmic reticulum stress during cerebral ischemia, is a major cause if intracellular calcium overload. Therefore, the timely recovery of intracellular calcium homeostasis , become an important part of treatment of ischemic stroke .
Keywords： Pharmacology; Ischemic stroke; Calcium overload 

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