文献类型：期刊文献

英文题名：Curcumin attenuates amyloid-beta-induced tau hyperphosphorylation in human neuroblastoma SH-SY5Y cells involving PTEN/Akt/GSK-3 beta signaling pathway

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

第一作者：黄汉昌

通讯作者：Huang, HC[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Beijing Union Univ, Coll Arts & Sci, Beijing 100191, 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 West Rd, Beijing 100191, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;

年份：2014

卷号：34

期号：1

起止页码：26-37

外文期刊名：JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION

收录：;Scopus(收录号：2-s2.0-84893118788);WOS:【SCI-EXPANDED(收录号:WOS:000330735600006)】；

基金：This study was supported by the National Natural Science Foundation of China (31071512) and the Scientific Research Common Program of Beijing Municipal Commission of Education (SQKM201411417003).

语种：英文

外文关键词：Amyloid-beta; Alzheimer's disease; curcumin; GSK-3 beta; PTEN; tau hyperphosphorylation

摘要：Accumulated amyloid-beta peptide (A beta) and hyperphosphorylated tau proteins are two hallmarks of Alzheimer's disease (AD). Increasing evidence suggests that A beta induces tau hyperphosphorylation in AD pathology, but the signaling pathway is not completely understood. Inhibiting A beta-induced cellular signaling is beneficent to AD treatment. In this study, cellular signaling of tau phosphorylation induced by A beta and the inhibiting effects of curcumin on this signaling were investigated on human neuroblastoma SH-SY5Y cells. The results indicated that curcumin inhibits A beta-induced tau phosphorylation at Thr231 and Ser396, over-expression of HDAC6, and decrease in phosphorylation of glycogen synthase kinase-3 beta (GSK-3 beta) at Ser9. However, the protective effect of curcumin on dephosphorylation of GSK-3 beta induced by A beta is not directly related to cellular oxidative stress. Curcumin depresses A beta-induced down-regulation of phosphorylations of Akt at Thr308 and Ser473 and 3-phosphoinositide-dependent protein kinase 1 at Ser241, implying that second message PIP3 involves curcumin-protective cell signaling. Furthermore, insulin receptor/phosphatidyl inositol 3-kinase pathway, as a regulatory signaling of second message PIP3, does not participate in A beta-induced deactivation of Akt (dephosphorylation at Thr308 and Ser473). However, A beta results in over-expression of Phosphatase and tensin homolog (PTEN), a negative regulator of PIP3. Curcumin depresses A beta-induced up-regulation of PTEN induced by A beta. These results imply that curcumin inhibits A beta-induced tau hyperphosphorylation involving PTEN/Akt/GSK-3 beta pathway.