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  • 标题:Induction of Apoptosis and Cytotoxicity by Isothiocyanate Sulforaphene in Human Hepatocarcinoma HepG2 Cells
  • 本地全文:下载
  • 作者:Saie Brindha Kntayya ; Muhammad Din Ibrahim ; Nooraini Mohd Ain
  • 期刊名称:Nutrients
  • 电子版ISSN:2072-6643
  • 出版年度:2018
  • 卷号:10
  • 期号:6
  • 页码:718
  • DOI:10.3390/nu10060718
  • 语种:English
  • 出版社:MDPI Publishing
  • 摘要:Glucoraphenin, a glucosinolate present in large quantities in radish is hydrolysed by myrosinase to form the isothiocyanate sulforaphene, which is believed to be responsible for its chemopreventive activity; however, the underlying mechanisms of action have not been investigated, particularly in human cell lines. The aim of the study is to assess the cytotoxicity of sulforaphene in HepG2 cells and evaluate its potential to enhance apoptosis. The cytotoxicity of sulforaphene in HepG2 cells was carried out ensuing an initial screening with two other cell lines, MFC-7 and HT-29, where sulforaphene displayed highest toxicity in HepG2 cells following incubation at 24, 48 and 72 h. In contrast, the intact glucosinolate showed no cytotoxicity. Morphological studies indicated that sulforaphene stimulated apoptosis as exemplified by cell shrinkage, blebbing, chromatin condensation, and nuclear fragmentation. The Annexin V assay revealed significant increases in apoptosis and the same treatment increased the activity of caspases -3/7 and -9, whereas a decline in caspase-8 was observed. Impairment of cell proliferation was indicated by cell cycle arrest at the Sub G0/G1 phase as compared to the other phases. It may be concluded that sulforaphene, but not its parent glucosinolate, glucoraphenin, causes cytotoxicity and stimulates apoptosis in HepG2 cells.
  • 关键词:glucoraphenin; sulforaphene; HepG2 cells; apoptosis; cell cycle arrest glucoraphenin ; sulforaphene ; HepG2 cells ; apoptosis ; cell cycle arrest
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