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机构地区:[1]广东医学院医学检验研究所 [2]广东医学院生物化学与分子生物学研究所,广东湛江524023
出 处:《中国药理学通报》2009年第2期217-221,共5页Chinese Pharmacological Bulletin
基 金:广东省重点学科资助项目(No0508);广东省中医药局资助课题(No2007129);湛江市科技计划资助项目(No2004003)
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。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 mR- NA expression of p21, CDK4, E2F1 and bax were detected by RT-PCR and Western blot respectively. Resuits 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. Conclu- sion 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.
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