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急性肾衰(ARF)发病机制尚未完全阐明,近来资料表明钙超载在ARF发病中起着重要的作用。而过多Ca2+是通过与其受体蛋白钙调素(Calmodulin,CaM)结合而起作用的,所以通过阻断Ca2+内流和(或)抑制CaM活性可减轻或抑制细胞死亡从而起到保护作用。为了解CaM拮抗剂(CaMA)对ARF的保护作用
The pathogenesis of acute renal failure (ARF) has not yet been fully elucidated, and recent data suggest that calcium overload plays an important role in the pathogenesis of ARF. Too much Ca2 + plays a protective role by binding to its receptor protein Calmodulin (CaM), so it can play a protective role by blocking Ca2 + influx and / or inhibiting CaM activity to reduce or inhibit cell death. To understand the protective effects of CaM antagonists on ARF