Effect of ginsenoside Rh2 on transplanted-tumor and expression of JAM in mice.
- Author:
Qiang WANG
1
;
Mei-Qing WU
;
Ling-Hui ZHAO
;
Hui-Ke YANG
;
Xiao-Hong LV
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Adhesion Molecules; metabolism; Drugs, Chinese Herbal; pharmacology; Female; Gene Expression Regulation; drug effects; Ginsenosides; pharmacology; Immunoglobulins; metabolism; Immunohistochemistry; Male; Mice; Neoplasm Transplantation; Neoplasms; metabolism; pathology; Receptors, Cell Surface; metabolism
- From: China Journal of Chinese Materia Medica 2008;33(18):2116-2119
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo discuss the anti-tumor activity of ginsenoside Rh2, we observed the expressions of the junction adhesion molecul (JAM) in transplanted-tumor in mice.
METHODThe models of 40 transplanted-tumor mice that were established by subsequently injecting cancer ascite of mice (S180) with 0.2 mL per mouse into the preepipodite skin were divided into two groups. Experiment group was drenched with 2 mL ginsenoside Rh2 per mouse, equating to a dose 20 mg x kg(-1). Control group was drenched with 2 mL normal saline per mouse. The expression of JAM-1, JAM-2 in the lymphatics, blood vessels and tumours were observed by immunohistochemical staining.
RESULTThe expression of JAM-1 on the cancer cells was significantly decreased in experiment group (IA 340.55) as compared with control group (IA 549.90, P<0.05). However, JAM-2 weakly expressed in both two groups. The density of blood vessels in which JAM-1, JAM-2 expressed showed 2.33 and 1.34 in control group, and 1.09 and 0.9 in experiment group respectively. Moreove, the density of lymph vessels were respectively 2.23 and 1.88 in control group compared with 0.99 and 0.79 in experiment group. The expression in blood vessels and lymph vessels in control group were significantly higher than those in experiment group, respectively (P<0.05).
CONCLUSIONGinsenoside Rh2 can affect the tumor growth, further angiogenesis and lymphangiogenesis by down-regulating JAM expression in tumor.