Effect of captopril on AGS nude mouse model of gastric cancer
10.3969/j.issn.1000-4718.2014.04.011
- VernacularTitle:卡托普利对 AGS 胃癌裸鼠移植瘤模型的调控作用
- Author:
Li LI
;
Zhendong JIN
;
Min CAI
;
Bin WANG
;
Fengtao CHENG
- Publication Type:Journal Article
- Keywords:
Captopril;
Stomach neoplasms;
Nude mice
- From:
Chinese Journal of Pathophysiology
2014;33(4):635-639
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To observe the effect of captopril on the genesis and development of gastric cancer , and to explore its clinical treatment feasibility for gastric cancer .METHODS:The human gastric cancer cell line AGS was used to establish a tumor model in nude mice , and the model mice were randomly divided into 3 groups: positive control ( 5-fluorouracil) group, normal control (saline) group and experimental (captopril) group.After intraperitoneal injection or intragastric administration of the drugs , the tumor growth curve was determined , and the tumor tissues were also sampled to detect the expression of Ki-67, STAT3, Bax and Bcl-2 by real-time quantitative PCR and immunohistochemistry .The apop-tosis was detected by TUNEL +DAPI staining .RESULTS: The tumor growth curve showed that the tumor model in the nude mice was successfully established .The tumor volumes among groups showed significantly different after 14 d growth. The increase in the tumor volume in normal control group was significantly faster than that in the other two groups , and that in positive control group was the slowest .The expression of Bax in captopril group increased , and the expression of STAT3, Ki-67 and Bcl-2 was reduced as compared with normal control group and positive control group .Compared with normal con-trol group, the apoptotic rate increased significantly , and the protein expression of p-STAT3 and STAT3 decreased obviously in positive control group and captopril group .CONCLUSION:With better feasibility , angiotensin-converting enzyme in-hibitor captopril has a significant effect on treating gastric cancer in the AGS nude mouse model by regulating the expression of STAT3, Bax, Bcl-2 and Ki-67 to accelerate the apoptosis of cancer cells , thus inhibiting tumor growth .
