文献类型：期刊文献

英文题名：Curcumin-Mediated Neuroprotection Against Amyloid-beta-Induced Mitochondrial Dysfunction Involves the Inhibition of GSK-3 beta

作者：Huang, Han-Chang[1,2];Xu, Ke[3];Jiang, Zhao-Feng[1]

第一作者：黄汉昌;Huang, Han-Chang

通讯作者：Jiang, ZF[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Beijing Univ Chem Technol, Coll Life Sci & Technol, Beijing, Peoples R China;[3]Capital Normal Univ, Coll Life Sci, Beijing, Peoples R China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, 197 Beitucheng W Rd, Beijing 100191, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2012

卷号：32

期号：4

起止页码：981-996

外文期刊名：JOURNAL OF ALZHEIMERS DISEASE

收录：;Scopus(收录号：2-s2.0-84871451491);WOS:【SCI-EXPANDED(收录号:WOS:000311227200010)】；

基金：This research was supported by National Natural Science Foundation of China (Grant No. 31071512), Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality (PHR(IHLB)) [PHR20090514], and Subsidy for Outstanding People of Beijing (Grant No. 2012D005022000006).

语种：英文

外文关键词：Alzheimer's disease; amyloid-beta; curcumin; glycogen synthase kinase-3 beta; mitochondrial dysfunction; reactive oxygen species

摘要：The deposition of amyloid-beta (A beta) peptides in senile plaques is one of pathological hallmarks of Alzheimer's disease (AD). Mitochondrial dysfunction is an early event of cell apoptosis. Increasing evidence indicates that A beta induces neuronal apoptosis through mitochondrial dysfunction. Curcumin, an anti-oxidative component of turmeric (Curcuma longa), has shown anti-tumor, anti-inflammatory, and anti-oxidative properties. In this study, we investigated the protective effects of curcumin against mitochondrial dysfunction induced by A beta. Based on the assay results of mitochondrial metabolic markers, we found that curcumin protects human neuroblastoma SH-SY5Y cells against the A beta-induced damage of mitochondrial energy metabolism. Curcumin inhibits A beta-induced mitochondrial depolarization of membrane potential (Delta psi(m)) and suppresses mitochondrial apoptosis-related proteins including cytochrome c, caspase-3, and Bax, which are activated by A beta. A beta-induced disturbances of redox state are linked to mitochondrial dysfunction. Curcumin normalizes cellular antioxidant enzymes (including SOD and catalase) in both protein expression and activity and decreases oxidative stress level in A beta-treated cells. Both total GSK-3 beta expression and phospho-Ser9 GSK-3 beta (pSer9-GSK-3 beta) are down-regulated in the cells pre-treated with curcumin. This study demonstrates curcumin-mediated neuroprotection against A beta-induced mitochondrial metabolic deficiency and abnormal alteration of oxidative stress. Inhibition of GSK-3 beta is involved in the protection of curcumin against A beta-induced mitochondrial dysfunction.