Jang Young Jin, Kim Jong-Eun, Kang Nam Joo, Lee Ki Won, Lee Hyong Joo
Major in Biomodulation, Department of Agricultural Biotechnology, Seoul National University, Seoul, Korea.
Ann N Y Acad Sci. 2009 Aug;1171:176-82. doi: 10.1111/j.1749-6632.2009.04727.x.
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 micromol/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.
阿尔茨海默病（AD）是一种与年龄相关的神经退行性疾病，其中细胞凋亡可能起着重要作用。4-羟基壬烯醛（HNE）是氧化应激产生的主要脂质过氧化产物，其在AD大脑中的水平升高。在本研究中，浓度为20微摩尔/升的紫铆因（而非白藜芦醇）可抑制HNE诱导的PC12细胞死亡。用HNE处理可诱导PC12细胞核浓缩，而紫铆因处理可减轻这种现象。HNE诱导聚（ADP-核糖）聚合酶裂解并降低Bcl-2表达，这两种作用均被紫铆因减弱。紫铆因还抑制c-Jun氨基末端激酶的磷酸化，该激酶是HNE诱导PC12细胞死亡的关键调节因子。这些结果表明紫铆因在预防AD方面具有治疗潜力。
