Effect of polypeptide extract from scorpion venom (PESV) on immune escape of Lewis lung carcinomas.
- Author:
Lin XU
1
;
Weidong ZHANG
;
Zhaopeng WANG
;
Qing JIA
;
Yueying ZHANG
;
Guosheng JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; B7-1 Antigen; immunology; B7-2 Antigen; immunology; Carcinoma, Lewis Lung; drug therapy; immunology; Disease Models, Animal; Humans; Interleukin-10; immunology; Lung Neoplasms; drug therapy; immunology; Male; Mice; Mice, Inbred C57BL; Peptides; administration & dosage; immunology; isolation & purification; Scorpion Venoms; chemistry; immunology; Tumor Escape; drug effects
- From: China Journal of Chinese Materia Medica 2010;35(17):2324-2327
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of polypeptide extract from scorpion venom (PESV) on immune escape of Lewis lung carcinomas (LLC) and its mechanism.
METHODForty C57BL/6J mice were inoculated with LLC cells suspension (1 x 10(7) cells/ mL) in right armpit subcutaneously. The tumor-bearing mice were randomly divided into two groups: the control group and the PESV group. PESV was intragastrically subjected to the mice of the experimental group for 18 days. The tumor volume and tumor inhibitory rate were determined. The expression levels of VEGF,TGF-beta1 and IL-10 in tumor microenvironment were determined by immunohisto-chemistry-staining and ELISA. Surface co-stimulatory molecules CD80 and CD86 of tumor infiltrating dendritic cells (DC) were determined by immunohistochemistry-staining and flow cytometry.
RESULTThe growth inhibitory rate of PESV was 56. 60%. The expression levels of VEGF,TGF-beta1 and IL-10 were decreased in tumor and serum, while the expression of co-stimulatory molecules CD80 and CD86 on DC were increased in tumor. Compared with the control group, the differences were all significant (P < 6.05).
CONCLUSIONPESV was effective in recovering immuno-surveillance and intervening immune escape of lung cancer through multi-pathway. And its effects might be attained by decreasing the level of VEGF, TGF-beta1 and IL-10 in tumor microenvironment and increasing the expression of co-stimulatory molecules CD80 and CD86 on DC.
