Wang J P, Teng C M
Pharmacological Institute, College of Medicine, National Taiwan University, Taipei.
Eur J Pharmacol. 1988 Nov 15;157(1):61-6. doi: 10.1016/0014-2999(88)90471-2.
Trimucase II, a proteolytic enzyme isolated from Trimeresurus mucrosquamatus venom, caused rat hind-paw edema dose dependently. Captopril potentiated significantly, while pretreatment with cellulose sulfate suppressed the trimucase II-induced edematous response. Pretreatment with diphenhydramine and methysergide reduced by 42 and 46% the edema induced by trimucase II and kallikrein, respectively. The residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin and trasylol. Kinin generation by trimucase II was also found in vitro from plasma and was concentration- and time-dependent. Kinin formation was inhibited by soybean trypsin inhibitor, trasylol and endogenous kininase. The kinins released were destroyed by chymotrypsin. Unlike cellulose sulfate, trimucase II caused kinin formation from Factor XII-deficient and prekallikrein-deficient plasma but not from high molecular weight kininogen-deficient plasma. These data indicate that, in addition to the mediators released from mast cells, kinins have an important role in the edema caused by trimucase II, and that kinins are released from plasma, probably due to direct activation of kininogen.
竹叶青蛋白酶II是从竹叶青蛇毒中分离出的一种蛋白水解酶，可引起大鼠后爪剂量依赖性水肿。卡托普利可显著增强其作用，而用硫酸纤维素预处理则可抑制竹叶青蛋白酶II诱导的水肿反应。用苯海拉明和甲基麦角新碱预处理分别使竹叶青蛋白酶II和激肽释放酶诱导的水肿减少42%和46%。[Thi⁵,⁸,D-Phe⁷]缓激肽和抑肽酶可使残余反应进一步显著降低。在体外也发现竹叶青蛋白酶II可使血浆生成激肽，且呈浓度和时间依赖性。激肽的形成受到大豆胰蛋白酶抑制剂、抑肽酶和内源性激肽酶的抑制。释放出的激肽被糜蛋白酶破坏。与硫酸纤维素不同，竹叶青蛋白酶II可使缺乏因子XII和前激肽释放酶的血浆生成激肽，但不能使缺乏高分子量激肽原的血浆生成激肽。这些数据表明，除了肥大细胞释放的介质外，激肽在竹叶青蛋白酶II引起的水肿中起重要作用，且激肽可能是由于激肽原的直接激活而从血浆中释放出来的。
