Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0370220030470030159
Yakhak Hoeji
2003 Volume.47 No. 3 p.159 ~ p.166
Immunostimulation Activity of the Crude Polysaccharides Fractionated from Eleutherococcus senticosus, and its Application to Prevent of Tumors by Combination Therapy with Cisplatin
ÇÏÀº¼÷/Ha ES
Ȳ¼öÇö/À¯±¤¿ø/½Å±¤¼ø/Á¶Çü¹Î/±èâÇÑ/¹Ú¿ì¹®/À±ÅÃÁØ/Hwang SH/Yu KW/Shin KS/Cho HM/Kim CH/Park WM/Yoon TJ
Abstract
In order to study the clinical usefulness of crude polysaccharides fractionated from Eleutherococcus senticosus, EN-3, in eliminating tumors, we have investigated the e ffect of combination therapy on the murine tumor metastasis and growth models. In experimental metastasis of colon26-M3.1 cells, prophylactic intravenous (I.v.) administration of EN-3 (0.5, 5, and 50 ¥ìg/mouse) inhibited tumor metastasis compared with tumor control group in 33.6, 66.8, and 81.8% respectively, The administration of EN-3 (50 ¥ìg/mouse) also exhibited a 66.1% therapeutic effect on lung tumor metastasis. Although EN-3 induced no toxic effect on both tumor cell and normal splenocyte in the concentration below 100 ¥ìg/ml in in vitro, it induced significant proliferating activity on normal splenocyte in the concentration- dependent manner, In an analysis of NK-cell activity, I.v. adminisuation of EN-3 (4~100 ¥ìg/mouse) significantly augmented NK cytotoxicity to YAC-1 tumor cells. The combination treatments of cisplatin (10 ¥ìg) and EN-3 (5 ¥ìg) induced synergistic effect on the inhibition of tumor metastasis in experimental tumor metastasis model produced by colon26-M3.1 cells. In addition, the combination treatments also exhibited prolongation of lifespan in S-180 tumor bearing mouse for over the 60 days. Even though cisplatin (2.5 ¥ìg/ml) exhibited cytotoxicity to tumor cells and inhibited tumor growth over 95% in in vitro, combination treatment with EN-3 (20 ¥ìg/ml) was induced splenocyte proliferation and produced cytokines, such as TNF- ¥á, IL-1 and IL-12, from the macmphages. These results suggested that EN-3 stimulate immune system non-specifically and apply to the biological response modifiers (BRM) in chemoimmunotherapy for tumor prevention.
KEYWORD
FullTexts / Linksout information
Listed journal information
ÇмúÁøÈïÀç´Ü(KCI)