Mori H, Mihara M, Teshima K, Uesugi U, Xu Q, Sakamoto O, Koda A
Department of Pharmacology, Gifu Pharmaceutical University, Japan.
Int J Immunopharmacol. 1987;9(8):881-92. doi: 10.1016/0192-0561(87)90004-x.
OK-432, a lyophilized preparation of Streptococcus pyogenes, showed a priming activity for TNF production in mice, associated with an increase of spleen weight. PSK, a protein-bound polysaccharide preparation from Coriolus versicolor, did not show such activity. Both OK-432 and PSK potentiated the TNF production in mice primed with Corynebacterium parvum (CP) and challenged with Escherichia coli endotoxin (LPS). Cytotoxic antitumor agents of 5-fluorouracil (5-FU), cyclophosphamide (CY) and bleomycin (BLM) suppressed TNF production in mice primed with CP and challenged with LPS. TNF production suppressed by 5-FU, CY and BLM was partially restored by the combined treatment with OK-432 or PSK. These results suggest that the administration of cytotoxic antitumor agents suppresses the intrinsic TNF production in cancer patients, and the combined use of immunostimulants such as OK-432 and PSK is advantageous in restoring TNF production suppressed by cytotoxic antitumor agents.
OK-432是化脓性链球菌的冻干制剂，对小鼠肿瘤坏死因子（TNF）的产生具有启动活性，这与脾脏重量增加有关。PSK是一种从云芝中提取的蛋白结合多糖制剂，不具有这种活性。OK-432和PSK均可增强经短小棒状杆菌（CP）致敏并受到大肠杆菌内毒素（LPS）攻击的小鼠的TNF产生。5-氟尿嘧啶（5-FU）、环磷酰胺（CY）和博来霉素（BLM）等细胞毒性抗肿瘤药物可抑制经CP致敏并受到LPS攻击的小鼠的TNF产生。5-FU、CY和BLM抑制的TNF产生可通过与OK-432或PSK联合治疗得到部分恢复。这些结果表明，细胞毒性抗肿瘤药物的给药会抑制癌症患者体内内源性TNF的产生，而联合使用OK-432和PSK等免疫刺激剂有利于恢复被细胞毒性抗肿瘤药物抑制的TNF产生。
