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姜黄素影响Aβ_(25-35)诱导PC12细胞周期变化与细胞凋亡的可能机制
引用本文:谢朝阳,祝其锋,吴斌华.姜黄素影响Aβ_(25-35)诱导PC12细胞周期变化与细胞凋亡的可能机制[J].中国药理学通报,2009,25(2).
作者姓名:谢朝阳  祝其锋  吴斌华
作者单位:1. 广东医学院医学检验研究所,广东,湛江,524023
2. 广东医学院生物化学与分子生物学研究所,广东,湛江,524023
基金项目:广东省重点学科资助项目,广东省中医药局资助课题,湛江市科技计划 
摘    要:目的探讨姜黄素(curcum in,Cur)对β-淀粉样肽(25-35)β-amyloidpeptide-(25-35),Aβ25-35]诱导体外血清饥饿培养的PC12细胞周期异常与凋亡保护作用的可能机制。方法5μmol.L-1Cur预处理同步于G0期的PC12细胞,加入终浓度为25μmol.L-1Aβ25-35处理0~20h,用RT-PCR和Western blot从mRNA及蛋白水平检测p21、CDK4、E2F1、bax的表达。结果与Aβ25-35诱导组比较,Cur保护组p21mRNA和p21蛋白的表达增加;CDK4、E2F1、baxmRNA和CDK4、Bax蛋白的表达降低。结论Cur可能通过上调p21的表达,下调CDK4、E2F1、bax的表达,对Aβ25-35诱导的PC12细胞周期异常与凋亡起保护作用。

关 键 词:姜黄素  Aβ_(25-35)  PC12细胞  基因表达  p21  CDK4  E2F1  Bax

Effective mechanism of curcumin on abnormal cell cycle and apoptosis of serum-deprived PC12 cells induced by β-amyloid peptide(25-35)
XIE Zhao-yang,ZHU Qi-feng,Wu Bin-hua.Effective mechanism of curcumin on abnormal cell cycle and apoptosis of serum-deprived PC12 cells induced by β-amyloid peptide(25-35)[J].Chinese Pharmacological Bulletin,2009,25(2).
Authors:XIE Zhao-yang  ZHU Qi-feng  Wu Bin-hua
Abstract:Aim To study the effective mechanism of curcumin on abnormal cell cycle and apoptosis of serum-deprived PC12 cells induced by β-amyloid peptide 25-35(Aβ25-35).Methods Synchronized PC12 cells were pretreated with 5 μmol·L-1 Cur for 1 h,and then 25 μmol·L-1 Aβ25-35 for 24 h.Protein and mRNA expression of p21,CDK4,E2F1 and bax were detected by RT-PCR and Western blot respectively.Results After synchronized PC12 cells being pretreated with 5 μmol·L-1 Cur for 1 h,the mRNA and protein expression of p21 gene were increased gradually,while CDK4,E2F1 and bax gene were decreased.Conclusion Cur maybe effects the redistribution of cell cycle and apoptosis of serum-deprived PC12 cells induced by Aβ25-35,through increasing the mRNA and protein expression of p21,and decreasing the mRNA and protein expression of CDK4,E2F1 and bax gene.
Keywords:p21  CDK4  E2F1  Bax
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