Xu Lin, Zhang Weidong, Wang Zhaopeng, Jia Qing, Zhang Yueying, Jiang Guosheng
Department of Experimental Pathology and Pathophysiology, Institute of Basic Medicine, Shandong Academy of Medical Sciences, China.
Zhongguo Zhong Yao Za Zhi. 2010 Sep;35(17):2324-7.
To study the effects of polypeptide extract from scorpion venom (PESV) on immune escape of Lewis lung carcinomas (LLC) and its mechanism.
Forty 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.
The 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).
PESV 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.
研究蝎毒多肽提取物（PESV）对Lewis肺癌（LLC）免疫逃逸的影响及其机制。
40只C57BL/6J小鼠右腋皮下接种LLC细胞悬液（1×10⁷细胞/mL）。将荷瘤小鼠随机分为两组：对照组和PESV组。对实验组小鼠进行18天的PESV灌胃。测定肿瘤体积和肿瘤抑制率。采用免疫组织化学染色和酶联免疫吸附测定法测定肿瘤微环境中VEGF、TGF-β1和IL-10的表达水平。采用免疫组织化学染色和流式细胞术测定肿瘤浸润树突状细胞（DC）表面共刺激分子CD80和CD86。
PESV的生长抑制率为56.60%。肿瘤组织和血清中VEGF、TGF-β1和IL-10的表达水平降低，而肿瘤中DC表面共刺激分子CD80和CD86的表达增加。与对照组相比，差异均有统计学意义（P<0.05）。
PESV可通过多途径有效恢复免疫监视并干预肺癌的免疫逃逸。其作用可能是通过降低肿瘤微环境中VEGF、TGF-β1和IL-10的水平，增加DC表面共刺激分子CD80和CD86的表达来实现的。
