摘要
研究了灵芝肽(GLP)在体外对人肝癌HepG2细胞凋亡的影响,并初步探讨了其作用机制。结果显示,透射电镜下可见细胞染色质浓缩、聚集于核边缘成块状,形成典型的凋亡小体;GLP使HepG2细胞阻滞于G0/G1期,随着GLP浓度升高,其G0/G1期的细胞比例随之增加;同时细胞的早期、晚期和总的凋亡率亦均随之增加,存在剂量-效应关系;Western blotting检测结果显示,抑制凋亡基因bcl-2和survivin表达下调,而促凋亡基因p53表达上调,并且都存在剂量依赖性;细胞凋亡的关键蛋白酶caspase-3被激活,并且caspase-3酶活性与GLP浓度亦有剂量依赖性。提示GLP体外可诱导人肝癌HepG2细胞凋亡,其作用机制可能与bcl-2和survivin表达下调、p53表达上调及Caspase-3被激活有关。
Apoptosis effects of human hepatoma HepG2 cells induced by Ganoderma lucidum peptides （GLP） in vitro were investigated. Apoptosis features were observed under transmission electron microscopy, including chromatin condensation, massive on the nuclear edge and formation of typical apoptotic bodies. GLP could lead to HepG2 cells arrest in G0/G1 cell cycle, and the cell proportion of G0/G1 phase increased as the increase of GLP concentration, meanwhile the apoptosis rate of early stage, late stage and total rate of apoptosis also increased in a dose dependent manner. The result of western blotting showed that the expression levels of bcl-2 and survivin, which were the apoptosis inhibiting genes, were down-regulated and p53, which was the apoptosis improving gene, was up-regulated in a dose dependent manner. The activity of caspase-3, which was key proteinase of cell apoptosis, was activated by GLP in a dose-dependent manner. It was suggested that GLP could induce HepG2 cells apoptosis, and the mechanism of GLP was probably associated with the down-regulation of bcl-2 and surviving expression, up-regulation of p53 expression and activation of caspase-3 activity.
出处
《菌物学报》
CAS
CSCD
北大核心
2010年第3期442-448,共7页
Mycosystema
基金
国家自然科学基金(No.30570190)
"十一五"国家科技支撑计划(No.2006BAD27B09-4)
关键词
药用真菌
寡肽
抗癌作用
凋亡机制
medicinal fungus
oligopeptide
anti-cancer action
apoptotic mechanism
