Effects of xiaotan sanjie recipe on vasculogenic mimicry of human gastric cancer xenografts in nude mice.
- Author:
Wei ZHOU
1
;
Yong-jin LI
;
Pin-kang WEI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Line, Tumor; Drugs, Chinese Herbal; pharmacology; Humans; Male; Matrix Metalloproteinase 2; metabolism; Matrix Metalloproteinase 9; metabolism; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Stomach Neoplasms; blood supply; metabolism; pathology; Xenograft Model Antitumor Assays
- From: Chinese Journal of Integrated Traditional and Western Medicine 2011;31(4):532-536
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of Xiaotan Sanjie Recipe (XTSJD) and its mechanism on vasculogenic mimicry (VM) of human gastric cancer xenografts in nude mice.
METHODSThe tumor-bearing mice model was established by subcutaneous inoculating with xenografts of human gastric cancer into the right armpit of 30 BALB/c nude mice. After modeling, the tumor-bearing mice were randomly divided into the normal saline group, the XTSJD group, and the doxycycline hyclate (DH) group, 10 in each. And the mice were administered with corresponding medicine by gastrogavage for 4 weeks. Then all mice were killed by cervical dislocation. The tumor mass were weighed and the tumor inhibition rate calculated. The amount of VM in tumor was counted. Expressions of matrix metalloproteinase (MMP) -2 and MMP-9 were tested using immunohistochemical method.
RESULTSTumor weight in the XTSJD group and the OH group decreased significantly when compared with the NS group (P<0.01). The amount of VM in the XTSJD group (24.50+/-3.03) and the OH group (14.70+/-1.34) was significantly less than that in the NS group (33.10+/-2.64) (P<0.01). The positive expressions of MMP-2 and MMP-9 in the XTSJD group and the OH group was significantly lower than that in the NS group (P <0.01).
CONCLUSIONXTSJD could inhibit the formation of VM in xenografted tumor of nude mice. The mechanism might be correlated with the down-regulation of MMP-2 and MMP-9 expressions.