Kobayashi H, Matsunaga K, Fujii M
Higashi-Nihon Gakuen University, Hokkaido, Japan.
Cancer Epidemiol Biomarkers Prev. 1993 May-Jun;2(3):271-6.
PSK, a protein-bound polysaccharide preparation obtained from cultured mycelia of the CM-101 strain of Coriolus versicolor belonging to basidiomycetes, is a biological response modifier capable of exhibiting diverse biological activities. This agent has been used clinically for the treatment of postoperative cancer patients in Japan by oral use. In this paper, chemopreventive aspects of PSK were reviewed. Oral administration of PSK reduced the incidence of tumor and/or prolonged the survival period in the following chemical carcinogen-induced, radiation-induced, and spontaneously developed animal cancer models: rat gastrointestinal cancer induced by 1,2-dimethylhydrazine; rat hepatoma by 3'-methyl-dimethylaminobenzene; mouse thymic lymphoma by whole-body irradiation; mouse spontaneous mammary tumor; and so on. PSK did not interact and/or inhibit drug-metabolizing enzymes and had no effect on the Ames test. On the other hand, this agent scavenged active oxygen through the induction of manganese superoxide dismutase, prevented the increase in frequency of anticancer agent-induced sister chromatid exchange, and suppressed fetal deformation induced by transplacental injection of teratogen, suggesting an effect on the initiation or promotion process of carcinogenesis. Also, PSK regulated cytokine production and enhanced the antitumor activity of effector cells such as killer T-cells and natural killer cells, suggesting an effect on the growth process after the development of malignant cells. Thus, this agent seems to act at multiple steps during carcinogenesis rather than a particular step. The main mechanism may be an antiteratogenic effect attributed to radical trapping, preventive effects against chromosome injury, and immunomodulative effects attributed to the modulation of cytokine production and effector cell function.(ABSTRACT TRUNCATED AT 250 WORDS)
PSK是一种从属于担子菌纲的云芝CM - 101菌株培养菌丝体中获得的蛋白结合多糖制剂,是一种能够展现多种生物活性的生物反应调节剂。该制剂在日本已被临床用于口服治疗癌症术后患者。本文综述了PSK的化学预防作用。在以下化学致癌物诱导、辐射诱导和自发形成的动物癌症模型中,口服PSK可降低肿瘤发生率和/或延长生存期:1,2 - 二甲基肼诱导的大鼠胃肠道癌;3'-甲基 - 二甲基氨基苯诱导的大鼠肝癌;全身照射诱导的小鼠胸腺淋巴瘤;小鼠自发性乳腺肿瘤等。PSK不与药物代谢酶相互作用和/或抑制药物代谢酶,对艾姆斯试验无影响。另一方面,该制剂通过诱导锰超氧化物歧化酶清除活性氧,防止抗癌剂诱导的姐妹染色单体交换频率增加,并抑制经胎盘注射致畸剂诱导的胎儿畸形,提示其对致癌作用的启动或促进过程有影响。此外,PSK调节细胞因子产生并增强效应细胞如杀伤性T细胞和自然杀伤细胞的抗肿瘤活性,提示其对恶性细胞形成后的生长过程有影响。因此,该制剂似乎在致癌过程的多个步骤而非特定步骤起作用。主要机制可能是自由基捕获导致的抗致畸作用、对染色体损伤的预防作用以及细胞因子产生和效应细胞功能调节导致的免疫调节作用。(摘要截选至250字)