Shibuya M, Kawachi S, Aoyama A, Murata A, Baba M, Hirata K, Ohtsuka M, Matsusaka M, Yano T, Niitani H
Gan To Kagaku Ryoho. 1987 Jul;14(7):2286-92.
The antimetastatic effects of defibrinogenation with batroxobin were investigated in normal mice and in mice with depressed or activated natural killer (NK) cell activity. Batroxobin inhibited the formation of lung metastases after intravenous inoculation of the F10 subline of B16 melanoma. Inhibition of NK activity by treatment of mice with anti-asialo GM1 antibody abrogated the antimetastatic effects of Batroxobin. Conversely, augmentation of NK cell activity by poly I:C plus treatment with batroxobin produced additive antimetastatic effects. Studies on the mechanism of interaction between Batroxobin and NK cells revealed that Batroxobin treatment did not affect splenic NK activity in vitro. From these data, it was found that the antimetastatic effects of batroxobin are dependent on the level of NK activity in the host.
研究了巴曲酶去纤维蛋白作用对正常小鼠以及自然杀伤（NK）细胞活性降低或增强的小鼠的抗转移效果。巴曲酶抑制静脉接种B16黑色素瘤F10亚系后肺转移灶的形成。用抗唾液酸GM1抗体处理小鼠抑制NK活性可消除巴曲酶的抗转移作用。相反，聚肌胞苷酸联合巴曲酶处理增强NK细胞活性可产生相加的抗转移作用。对巴曲酶与NK细胞相互作用机制的研究表明，巴曲酶处理在体外不影响脾脏NK活性。从这些数据发现，巴曲酶的抗转移作用取决于宿主NK活性水平。
