Kawatsu M, Yamashita T, Ishizuka M, Takeuchi T
Insitute for Chemotherapy, M.C.R.F., Shizuoka, Japan.
Anticancer Res. 1997 Mar-Apr;17(2A):917-22.
The effect of conagenin (CNG) on the production of the inflammatory mediators induced by 5-fluorouracil (5-Fu) in mice was investigated. We found that the production of interleukin (IL)-1 alpha and prostaglandin E2(PGE2) in whole spleen cell cultures from mice given a sublethal dose of 5-Fu was induced in the week after treatment, and subsequently the production of IL-4 and IL-IO was induced. The administration of 5-Fu and CNG suppressed the production of IL-1 alpha and PGE2, and induced the production of IL-4 and IL-10 earlier than 5-Fu alone did. In cultures of cells from Peyer's patches, IL-1 alpha production was suppressed by CNG administration. The effect of CNG was also demonstrated in vitro. CNG at 0.001 to 1.0 microgram/ml suppressed IL-1 alpha and PGE2 production in cultures of adherent peritoneal exudate cells (PEC) and cells from Peyer's patches of mice given 5-Fu. IL-10 production in cultures of non-adherent splenic cells was enhanced by CNG. These results indicate that CNG modulates inflammatory responses induced by 5-Fu through production of anti-inflammatory cytokines such as IL-4 and IL-10.
研究了柯纳皂苷元（CNG）对5-氟尿嘧啶（5-Fu）诱导的小鼠炎症介质产生的影响。我们发现，给予亚致死剂量5-Fu的小鼠全脾细胞培养物中，白细胞介素（IL）-1α和前列腺素E2（PGE2）的产生在治疗后一周被诱导，随后IL-4和IL-10的产生被诱导。5-Fu与CNG联合给药抑制了IL-1α和PGE2的产生，并且比单独使用5-Fu更早地诱导了IL-4和IL-10的产生。在派尔集合淋巴结细胞培养物中，给予CNG可抑制IL-1α的产生。CNG的作用在体外也得到了证实。0.001至1.0微克/毫升的CNG可抑制给予5-Fu的小鼠腹腔黏附性渗出细胞（PEC）和派尔集合淋巴结细胞培养物中IL-1α和PGE2的产生。CNG可增强非黏附性脾细胞培养物中IL-10的产生。这些结果表明，CNG通过产生IL-4和IL-10等抗炎细胞因子来调节5-Fu诱导的炎症反应。
