Potential proconvulsant effects of oral zinc supplementation–A case report

详细信息	查看全文 | 推荐本文 |

• 作者：A. Laine Green ; Donald F. Weaver
• 关键词：Zinc ; Seizure ; Epilepsy
• 刊名：Neurotoxicology
• 出版年：2008
• 期刊代码：35_0161813x
• 类别：pha
• 出版时间：May 2008
• 卷：29
• 期：3
• 页码：476-477
• 文件大小：105 K

摘要

We examined the effect of (−)-syringaresinol, a furofuran-type lignan isolated from Daphne genkwa, on cell cycle regulation in HL-60 human promyelocytic leukemia cells in vitro. (−)-Syringaresinol decreased the viability of HL-60 cells by inducing G₁ arrest followed by apoptosis in a dose- and time-dependent manner. The G₀/G₁ phase of the cell cycle is regulated by cyclin-dependent kinases (Cdk), cyclins and cyclin-dependent kinase inhibitors (Cdki). We show by western blot analysis, that the (−)-syringaresinol-induced G₁ arrest was mediated through the increased expression of Cdki proteins (p21^cip1/waf1 and p27^kip1) with a simultaneous decrease in cdk2, cdk4, cdk6, cyclin D₁, cyclin D₂, and cyclin E expression. The induction of apoptosis after treatment with (−)-syringaresinol for 24 h was demonstrated by morphological changes, DNA fragmentation, altered ratio of Bax/Bcl-2, cleavage of poly(ADP-ribose) polymerase and flow cytometry analysis. (−)-Syringaresinol also induced cytochrome c release and activation of caspase-3 and caspase-9. To our knowledge, this is the first time that (−)-syringaresinol has been reported to potently inhibit the proliferation of human promyelocytic HL-60 cells through G₁ arrest and induction of apoptosis. These findings suggest that (−)-syringaresinol may be a potential chemotherapeutic agent for the treatment of cancer.