Piceatannol Attenuates 4-Hydroxynonenal-Induced Apoptosis of PC12 Cells by Blocking Activation of c-Jun N-Terminal Kinase
Piceatannol Attenuates 4-Hydroxynonenal-Induced Apoptosis of PC12 Cells by Blocking Activation of c-Jun N-Terminal Kinase
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DOI：
10.1111/j.1749-6632.2009.04727.x
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发表时间：
2009-01-01
期刊：
影响因子：
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通讯作者：
Lee, Hyong Joo
中科院分区：
文献类型：
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作者：
Jang, Young Jin;Kim, Jong-Eun;Lee, Hyong Joo
阿尔茨海默病（AD）是一种与年龄相关的神经退行性疾病，细胞凋亡在其中起着潜在的重要作用。4-羟基壬烯醛（HNE）是氧化应激产生的主要脂质过氧化产物，其水平在AD脑中升高。在本研究中，白藜芦醇（而不是白藜芦醇）在20 μ mol/L的浓度抑制HNE诱导的PC 12细胞死亡。用HNE处理诱导PC 12细胞核凝聚，并且这被云杉醇处理减弱。HNE诱导的聚（ADP-核糖）聚合酶切割和Bcl-2的表达下降，这两种影响被减弱的云杉醇。Piceatannol还抑制c-Jun N-末端激酶的磷酸化，这是HNE诱导的PC 12细胞死亡的关键调节因子。这些结果表明，Piceatannol在预防AD方面具有治疗潜力。
Alzheimer's disease (AD) is an age-related neurodegenerative disorder in which apoptosis plays a potentially important role. 4-Hydroxynonenal (HNE) is a major lipid peroxidation product produced by oxidative stress, and its level is elevated in the AD brain. In the present study, piceatannol (but not resveratrol) at the concentration of 20 mu mol/L inhibited HNE-induced PC12 cell death. Treatment with HNE induced nuclear condensation in PC12 cells, and this was attenuated by piceatannol treatment. HNE induced poly(ADP-ribose) polymerase cleavage and decreased Bcl-2 expression, with both of these effects being attenuated by piceatannol. Piceatannol also inhibited the phosphorylation of c-Jun N-terminal kinase, which is a key regulator of HNE-induced PC12 cell death. These results indicate that piceatannol has therapeutic potential in the prevention of AD.