Hosseini Masoumeh Mansoubi, Karimi Aliasghar, Behroozaghdam Mitra, Javidi Mohammad Amin, Ghiasvand Saeedeh, Bereimipour Ahmad, Aryan Hoda, Nassiri Farbod, Jangholi Ehsan
Department of Microbiology, Faculty of Biological Science, North Tehran Branch, Islamic Azad University, Tehran, Iran.
Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
World Neurosurg. 2017 Dec;108:94-100. doi: 10.1016/j.wneu.2017.08.133. Epub 2017 Sep 1.
Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary cerebral tumor. The median survival time is 15 months despite maximum treatment because the tumor is resistant to most therapeutic modalities. Several studies have indicated chemopreventive and chemotherapeutic activity of cyanidin-3-glucoside (C3G) as an anthocyanin component. We aimed to illustrate the cytotoxic and apoptogenic effects of C3G in the U87 cell line (human GBM cell line).
Cytotoxic activity was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium assay after treatment with C3G at different concentrations in the U87 cell line. Cisplatin was used as a positive control for 24 and 48 hours. The percentage of apoptotic cells was determined using an Annexin V/propidium iodide assay, and the expression of bax, bcl2, and p53 genes was assessed using real-time polymerase chain reaction.
Treatment of U87 cells with 40 μg/mL of C3G resulted in 32% apoptotic cells after 24 hours. To further confirm that C3G treatment induced apoptosis in U87 cells, RNA expression of bax, bcl2, and p53 genes was investigated after treatment. Real-time polymerase chain reaction indicated that the expression of bax and p53 increased, whereas the expression of bcl2 decreased.
C3G had an apoptogenic effect in the GBM cell line. New information regarding the therapeutic effects of C3G in GBM could ultimately lead to the production of new drugs.
多形性胶质母细胞瘤（GBM）是最常见且侵袭性最强的原发性脑肿瘤。尽管进行了最大限度的治疗，其平均生存时间仍为15个月，因为该肿瘤对大多数治疗方式具有抗性。多项研究表明，花青素成分矢车菊素 - 3 - 葡萄糖苷（C3G）具有化学预防和化疗活性。我们旨在阐明C3G对U87细胞系（人GBM细胞系）的细胞毒性和诱导凋亡作用。
在U87细胞系中用不同浓度的C3G处理后，使用3 -（4,5 - 二甲基噻唑 - 2 - 基）- 2,5 - 二苯基四氮唑溴盐比色法评估细胞毒性活性。顺铂用作24小时和48小时的阳性对照。使用膜联蛋白V/碘化丙啶测定法确定凋亡细胞的百分比，并使用实时聚合酶链反应评估bax、bcl2和p53基因的表达。
用40μg/mL的C3G处理U87细胞24小时后，导致32%的细胞凋亡。为进一步证实C3G处理可诱导U87细胞凋亡，处理后研究了bax、bcl2和p53基因的RNA表达。实时聚合酶链反应表明，bax和p53的表达增加，而bcl2的表达降低。
C3G对GBM细胞系具有诱导凋亡作用。关于C3G在GBM中治疗作用的新信息最终可能会促成新药的产生。
