海葵毒素对神经胶质瘤细胞的凋亡诱导作用  

Malignant glioma cells apoptosis induced by sea anemones (Phyllodiscus semoni) venom

作　　者：袁兆新[1] 孙明莉[2] 赵冰[1] 杨鑫[3] 孔晓霞[1] 张宏宇[1] 孙连坤[1] 康劲松[1] 

机构地区：[1]吉林大学基础医学院病理生理教研室 [2]吉林大学第一医院ICU,吉林长春130021 [3]吉林大学第二医院

出　　处：《中风与神经疾病杂志》2006年第5期594-596,插页,共4页Journal of Apoplexy and Nervous Diseases

摘　　要：目的研究从海葵组织中提取的海葵毒素(Phyllodiscus semonii toxin,PsTX)对人神经胶质瘤细胞(U251)凋亡的诱导作用及其可能机制。方法MTT法检测PsTX对肿瘤细胞的增殖抑制率;原位末端脱氧核糖苷肽转移酶分析法(TUNEL)及DNA Ladder法检测PsTX对肿瘤细胞的凋亡诱导作用;免疫组织化学染色显示Fas蛋白在U251细胞中的表达。结果PsTX对人神经胶质瘤细胞具有明显的生长抑制及促凋亡作用,PsTX诱导Fas在人神经胶质瘤细胞膜上表达增高。结论PsTX可能通过Fas途径诱导人神经胶质瘤细胞凋亡。Objective To investigate whether Phyllodiscus semonii toxin (PsTX) from sea anemone could induce apoptosis in human U251 malignant glioma cells and to elucidate the possible mechanism involved. Methods Cell viability was estimated by MTT assay. Apoptosis was evaluated using TdT (terminal deoxynucleoridyl transferase)-mediated dUTP nick-end labeling (TUNEL) method and DNA gel electrophoresis. Furthermore in order to study the mechanism of apoptosis induced by PsTX,the Fas protein expression was measured using cell immunostaining. Results PsTX had a cytotoxic effect on U251 glioma cells. The fragmented DNA and large numbers of cells became TUNEL positive in U251 cells treated with PsTX. The Fas protein expression increased in the treated U251 cells at 6h after administration of PsTX. Conclusion The PsTX might cause the apoptosis through increasing expression of Fas protein in the U251 glioma cells. It is suggested that PsTX is promising potential candidate for tumor therapy.

关 键 词：海葵毒素 凋亡 FAS蛋白 神经胶质瘤细胞 

分 类 号：R394.2[医药卫生—医学遗传学]