Ning Yun-Na, Zhang Wei-Dong, Wu Li-Cun
Key Laboratory for Modern Medicine and Technology of Shandong Province, Institute of Basic Medicine, Shangdong Academy of Medical Sciences, Jinan 250062.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Apr;32(4):537-42.
To explore the mechanism of polypeptide extract from scorpion venom (PESV) on promoting anti-tumor effects of cyclophosphamide (CTX).
The Lewis lung tumor model was established by subcutaneously implanting Lewis lung cells into C57BL/6 mice. The tumor-bearing mice were randomly divided into 4 groups, i. e., the model group, the cyclophosphamide (CTX) group, the polypeptide extract from scorpion venom (PESV) group, and the combination group (CTX + PESV), 10 mice in each group. The tumor growth curve was recorded. Changes of vascular endothelial growth factor-A (VEGF-A) and transforming growth factor-beta1 (TGF-beta1) expressions in the tumor microenvironment were detected using reverse transcription PCR and immunohistochemical assay. Changes of dendritic cells (DCs) phenotype CD80 and CD86 expressions in the tumor tissue were detected using immunofluorescence chemical assay.
After 21 successive days of treatment, the growth of Lewis lung cancer transplantation tumor in the combination group was obviously inhibited (P<0.05). Compared with the model group,the expressions of CD80 and CD86 in the PESV group was somewhat enhanced, while those in the CTX group was somewhat lowered. Compared with the CTX group, the fluorescent signal strength and expressions in the combination group somewhat increased. Compared with the model group, the expressions of TGF-beta1 and VEGF-A mRNA decreased in the PESV group and the CTX group (both P<0.05). Compared with the PESV group and the CTX group, the expressions of TGF-beta1 and VEGF-A in the combination group both decreased (both P<0.05).
PESV could inhibit the expressions of VEGF and TGF-beta1, promote the maturation of DCs, recover its antigen uptake presentation function, and reverse the immune injury to the body by CTX, thus playing a role in inducing the tumor cell apoptosis.
探讨蝎毒多肽提取物（PESV）促进环磷酰胺（CTX）抗肿瘤作用的机制。
将Lewis肺癌细胞皮下接种于C57BL/6小鼠，建立Lewis肺癌模型。将荷瘤小鼠随机分为4组，即模型组、环磷酰胺（CTX）组、蝎毒多肽提取物（PESV）组和联合组（CTX + PESV），每组10只。记录肿瘤生长曲线。采用逆转录聚合酶链反应和免疫组织化学法检测肿瘤微环境中血管内皮生长因子-A（VEGF-A）和转化生长因子-β1（TGF-β1）表达的变化。采用免疫荧光化学法检测肿瘤组织中树突状细胞（DCs）表型CD80和CD86表达的变化。
连续给药21天后，联合组Lewis肺癌移植瘤生长明显受抑制（P<0.05）。与模型组比较，PESV组CD80和CD86表达有所增强，CTX组有所降低。与CTX组比较，联合组荧光信号强度及表达有所增加。与模型组比较，PESV组和CTX组TGF-β1和VEGF-A mRNA表达均降低（均P<0.05）。与PESV组和CTX组比较，联合组TGF-β1和VEGF-A表达均降低（均P<0.05）。
PESV可抑制VEGF和TGF-β1表达，促进DCs成熟，恢复其抗原摄取呈递功能，逆转CTX对机体的免疫损伤，从而发挥诱导肿瘤细胞凋亡的作用。
