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心肌再灌注损伤中细胞钙稳态与自由基生成之间的相互关系。

Interrelationship between cellular calcium homeostasis and free radical generation in myocardial reperfusion injury.

作者信息

Bagchi D, Wetscher G J, Bagchi M, Hinder P R, Perdikis G, Stohs S J, Hinder R A, Das D K

机构信息

Department of Surgery, Creighton University, Omaha, NE, USA.

出版信息

Chem Biol Interact. 1997 May 2;104(2-3):65-85. doi: 10.1016/s0009-2797(97)03766-6.

Abstract

This review describes the interrelationship between two important biological factors, intracellular calcium overloading and oxygen-derived free radicals, which play a crucial role in the pathogenesis of myocardial ischemic reperfusion injury. Free radicals are generated during the reperfusion of ischemic myocardium, and polyunsaturated fatty acids in the membrane phospholipids are the likely targets of the free radical attack. On the other hand, activation of phospholipases can provoke the breakdown of membrane phospholipids which results in the activation of arachidonate cascade leading to the generation of prostaglandins, and oxygen free radicals can be produced during the interconversion of the prostaglandins. In conclusion, it has been emphasized that the two seemingly different causative factors of reperfusion injury, intracellular calcium overloading and free radical generation are, in fact, highly interrelated.

摘要

本综述描述了两个重要生物学因素——细胞内钙超载和氧衍生自由基之间的相互关系,它们在心肌缺血再灌注损伤的发病机制中起关键作用。自由基在缺血心肌再灌注期间产生,膜磷脂中的多不饱和脂肪酸可能是自由基攻击的目标。另一方面,磷脂酶的激活可引发膜磷脂的分解,导致花生四烯酸级联反应的激活,进而产生前列腺素,且在前列腺素的相互转化过程中可产生氧自由基。总之,已经强调指出,再灌注损伤的两个看似不同的致病因素,即细胞内钙超载和自由基生成,实际上高度相关。

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