Holmberg S B, Naredi P L, Lindnér G O, Karlberg I H, Daneryd P L, Karlsson L M, Pettersson A, Stenram U, Hafström L R
Department of Surgery, Sahlgrenska Hospital, Göteborg, Sweden.
J Cancer Res Clin Oncol. 1995;121(8):463-8. doi: 10.1007/BF01218362.
Zymosan--a non-specific macrophage-stimulating agent--reduces tumour take in the liver. The mechanism for this effect is not clear, but it may be mediated via the Kupffer cells and prostaglandins. On the other hand, the Prostaglandin-synthesis inhibitor, indomethacin, inhibits tumour growth. Pretreatment with zymosan (3 mg 100 g-1) for 3 days of two different strains of rats, inoculated in the liver with a hepatoma or an adenocarcinoma cell suspension respectively, reduced tumour take and also initial tumour growth. The effect on tumour take and initial growth was inhibited by concomitant administration of indomethacin (0.2 mg 100 g-1). When zymosan was administered after tumour cell inoculation the growth rate of the hepatoma was retarded, but this effect was not abrogated by indomethacin. Pretreatment with indomethacin had no significant effect on tumour take or initial growth. When given after the tumour was established in the liver, indomethacin reduced the growth rate of the hepatoma, but not of the adenocarcinoma. These results suggest that there are different mechanisms for the effects of zymosan on tumour take and on growth of an established tumour. In immunoincompetent nude mice the effect on the hepatoma was similar to the effect in the rat. In vitro both tumours were insensitive to zymosan and indomethacin. This study confirms that pretreatment with a non-specific macrophage stimulator (zymosan) diminishes tumour take and growth in the liver, that the effect of zymosan on tumour take in the liver is abrogated by indomethacin and that the zymosan effect on tumour take in the liver is at least partly mediated by the Kupffer cells and prostaglandins.
酵母聚糖——一种非特异性巨噬细胞刺激剂——可减少肝脏肿瘤的发生。这种作用的机制尚不清楚，但可能是通过库普弗细胞和前列腺素介导的。另一方面，前列腺素合成抑制剂吲哚美辛可抑制肿瘤生长。分别用两种不同品系的大鼠，预先用酵母聚糖（3毫克/100克）处理3天，然后分别向其肝脏接种肝癌或腺癌细胞悬液，可减少肿瘤的发生以及初始肿瘤生长。吲哚美辛（0.2毫克/100克）同时给药可抑制对肿瘤发生和初始生长的影响。当在接种肿瘤细胞后给予酵母聚糖时，肝癌的生长速度会减慢，但吲哚美辛并不能消除这种作用。预先用吲哚美辛处理对肿瘤发生或初始生长没有显著影响。当在肝脏肿瘤形成后给予吲哚美辛时，可降低肝癌的生长速度，但对腺癌无效。这些结果表明，酵母聚糖对肿瘤发生和已形成肿瘤生长的影响存在不同机制。在免疫缺陷的裸鼠中，对肝癌的作用与在大鼠中的作用相似。在体外，两种肿瘤对酵母聚糖和吲哚美辛均不敏感。本研究证实，用非特异性巨噬细胞刺激剂（酵母聚糖）预处理可减少肝脏肿瘤的发生和生长，酵母聚糖对肝脏肿瘤发生的作用可被吲哚美辛消除，且酵母聚糖对肝脏肿瘤发生的作用至少部分是由库普弗细胞和前列腺素介导的。
