Zhao Xin-Can, Zhang Li, Yu Hui-Xin, Sun Zhen, Lin Xiu-Feng, Tan Chen, Lu Rong-Rong
Jiangsu Institute of Nuclear Medicine, Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, 20 Qian Rong Road, Wuxi, Jiangsu 214063, China; State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi, Jiangsu 214122, China.
Jiangsu Institute of Nuclear Medicine, Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, 20 Qian Rong Road, Wuxi, Jiangsu 214063, China.
Food Chem. 2011 Nov 15;129(2):387-394. doi: 10.1016/j.foodchem.2011.04.089. Epub 2011 May 4.
Curcumin has been traditionally used in China and India for food and medicinal purposes. It has been shown to possess potent antioxidative activity both in vitro and in vivo. In the present study, the neuroprotective effects and the potential mechanisms of curcumin against HO-induced oxidative stress in mouse neuroblastoma Neuro-2A cells were investigated. Treatment with curcumin at 20 and 25μg/mL for 1h prior to HO exposure significantly attenuated cell viability loss, reduced apoptosis, suppressed the elevation of intracellular reactive oxygen species (ROS) and calcium levels, and stabilised mitochondrial membrane potential. Furthermore, curcumin could block HO-mediated degradation of the protein IκBα and subsequent activation of nuclear factor κB, thus inhibiting the expression of its target gene cyclooxygenase 2. These results indicate that curcumin has potential protective effects against HO-induced oxidative stress in neuron cells, which might make curcumin a suitable therapeutic agent for prevention and treatment of neurodegenerative diseases associated with oxidative stress.
姜黄素在中国和印度传统上用于食品和医药用途。已表明其在体外和体内均具有强大的抗氧化活性。在本研究中,研究了姜黄素对小鼠神经母细胞瘤Neuro-2A细胞中血红素加氧酶(HO)诱导的氧化应激的神经保护作用及其潜在机制。在HO暴露前1小时用20和25μg/mL姜黄素处理,可显著减轻细胞活力丧失,减少细胞凋亡,抑制细胞内活性氧(ROS)水平和钙水平的升高,并稳定线粒体膜电位。此外,姜黄素可阻断HO介导的蛋白IκBα降解及随后的核因子κB激活,从而抑制其靶基因环氧化酶2的表达。这些结果表明,姜黄素对HO诱导的神经元细胞氧化应激具有潜在保护作用,这可能使姜黄素成为预防和治疗与氧化应激相关的神经退行性疾病的合适治疗剂。