飯匙倩心臟毒素對血小板的作用

Abstract

血小板經心臟毒素蛋白作用後，我們觀察到兩個現象: LDH的釋出及細胞骨架的變化。LDH的釋出表示血小板的細胞膜已遭到破壞。而早在細胞膜破損之前，細胞骨架已經發生了很大的變化，有許多原木以單體狀態存在於細胞質中之肌動蛋白聚合到細胞骨架上，使細胞骨架的肌動蛋白含量大增。 血小板若先以indomethacin處理，則CTX引起之LDH釋出量減少，此種效果可能是由於indomethacin抑制了細胞內PLA2的活性所致。但indomethacin無法抑制CTX引起之細胞骨架變化。反之，CB能抑制actin polymerization，因而抑制了細胞骨架的變化，卻對LDH的釋出毫無影響。因此，CTX對血小板的兩種作用，可能是經由不同的作用機制來達成。 Ca2＋能抑制CTX在血小板上引起的作用，亦會影響CTX在紅血球、心臟細胞、liposome上的作用，這可能是由於鈣離子興CTX之間的交互作用，而造成了CTX作用的減弱。

Cardiotoxin (CTX) from venom of Taiwan cobra (Naja naja atra) was found to increase the amount of actin in cytoskeleton of intack rabbit platelet within 10 seconds. Pretreatment of PLT with Cytochalasin B reduced the cytoskeletal actin of CTX-treated PLT to a level similar with that of control PLT, manifesting that cytoskeletal actin increase included actin polymerization. CTX also caused the leakage of lactate dehydrogenase, a cytoplasmic enzyme. Addition of indomethacin to PLT inhibited the leakage of LIDH caused by CTX to the extent of 50% without influencing the CTX-induced increase in cytoskeletal actin. Therefore, CTX may cause plasma membrane disruption and cytoskeletal structure change by different mechanisms. However, calcium ion inhibited both phenomena caused by CTX. Since Ca2+ also inhibited the action of CTX on RBC and heart cell, this inhibitive activity may come from the interaction between Ca2+ and CTX itself.