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A combination extract of Renshen(Panax Ginseng),Yinyanghuo(Herba Epimedii Brevicornus),Yuanzhi(Radix Palygalae) and Jianghuang(Rhizoma Curcumae Longae) decreases glycogen synthase kinase 3β expression in brain cortex of APPV717I transgenic mice

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Journal of Traditional Chinese Medicine 2013年第2期33卷 211-217页

作者： Jing Shi Jinzhou Tian Xuekai Zhang Chuiyou Zeng Mingqing Wei Pengwen Wang Yongyan Wang Department of Neurology Dongzhimen HospitalBeijing University of Chinese Medicine Clinical Neuroscience Research Group The University of ManchesterHope HospitalStott LaneSalfordManchester M6 8HDUK Key Laboratory of Chinese Internal Medicine Ministry of EducationBeijing University of Chinese Medicine Institute of Clinical Medicine China Academy of Chinese Medical Sciences

OBJECTIVE： To investigate the neuroprotective mechanism of combination extract of Renshen （Ponax Ginseng）, Yinyanghuo （Herba Epimedii Brevi-comus）, Yuanzhi （Radix Palygalae） and Jianghuang （Rhizoma Curcumae Longae）（GEPT） in treating AI- zheimer＇s disease on the target of glycogen syn- thase kinase 3β（GSK-3β）. METHODS： Three-month-old APPV7171 transgenic mice were randomly divided into ten groups （n=12 per group） and intragastrically administrated vehi- cle or medicines： APP group was given 0.5% CMC, donepezil group was given donepezil （APP ＋ D group）（0.92 mg/kg-1. day-1）, and GEPT groups were given small dose of GEPT （APP＋Gs group）（0.075 g/ kg-1. day-1）, medium dose （APP＋Gm group）（0.15 g/ kg-1. day-1）, and large dose （APP＋GI group）（0.30 g/ kg-1. day-1） for 4 or 8 months, respectively. Three-month-old C57BL/6J mice as vehicle controls （n=12） were given 0.5% CMC for 4 or 8 months as well. The GSK-3β expression in the cortex of 7- and 11-month-old APPV7171 transgenic mice with and without GEPT or donepezil treatment and normal C57BL/6J mice were measured via Western blotting and Immunohistochemistry. RESULTS： Immunohistochemistry analysis showed significant increase of GSK-3β in the cerebral cortex of 7-month-old APP group （compare to control group P=0.003）, while the GSK-313 expression of donepezil or OEPT group were all significantly de-creased （Donepezil vs APP： P=0.041; GI vs APP： P=0.049, Gm vs APP： P=0.029, Gh vs APP： P=0.036）. Western blot analysis showed similar results. The densitometric measures of GSK-3β in APP mice in- creased significantly as compared with the control group （P=0.008）. And the GSK-3β expression indonepezil and GEPT groups were all decreased. There was significant difference between Gh group or donepezil group and the control group （P=0.05）. Similar findings were shown in the 11-month-old mice in each group, except for greater decrease of GSK-3β in the GEPT group. CONCLUSION： GEPT can effectively decrease the level of GSK-3β expression

关键词： Alzheimer disease Mice, transgenic glycogen synthase kinase 3 Traditional ChineseMedicine Chinese medical formula

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Protection of INS-1 Cells from Free Fatty Acid-induced Apoptosis by Inhibiting the glycogen synthase kinase-3

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2007年第5期27卷 483-486页

作者：吴薇罗小平 Department of Pediatrics Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

To examine the role of glycogen synthase kinase 3 （GSK-3） in the apoptosis of pancreatic β-cells to better understand the pathogenesis and to find new approach to the treatment of type 2 diabetes, apoptosis was induced by oleic acid （OA） in INS-1 cells and the activity of GSK-3 was inhibited by LiCl. The PI staining and flow cytometry were employed for the evaluation of apoptosis. The phosphorylation level of GSK-3 was detected by Western blotting. The results showed that OA at 0.4 mmol/L could cause conspicuous apoptosis of INS- 1 cells and the activity of GSK-3 was significantly increased. After the treatment with 24 mmolFL of LiCl, a inhibitor of GSK-3, the OA-induced apoptosis of INS-1 cells was lessened and the phosphorylation of GSK-3 was increased remarkably. It is concluded that GSK-3 activation plays an important role in OA-induced apoptosis in pancreatic β-cells and inhibition of the GSK-3 activity can effectively protect INS-1 cells from the OA-induced apoptosis. Our study provides a new experimental basis and target for the clinical treatment of type-2 diabetes.

关键词： glycogen synthase kinase 3 apoptosis oleic acid

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glycogen synthase kinase-3β inhibition alleviates NLRP3 inflammasome activation in myocardial infarction

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中国药理学与毒理学杂志 2019年第10期 801-802页

作者： WANG Shu-hui XU Li-na SU Xue-ling MA Yu-ran ZHANG Li-rong HAN Sheng-na School of Basic Medical Sciences Zhengzhou University

OBJECTIVE To investigate the regulatory mechanisms of glycogen synthase kinase-3β(GSK-3β)on NLRP3 inflammasome activation. METHODS We conducted myocardial infarction(MI) model in male Sprague-Dawley(SD) rat during days 2-28. An in vitro investigation was performed using new-born rat/human cardiomyocyte and fibroblast cultures under typical inflammasome stimulation and hypoxia treatment. Further identification for possibility of GSK-3β active NLRP3 inflammasomes, GSK-3β immunoprecipitation was performed from the lysate of inflammasome stimulation-treated rat neonatal fibroblasts(RCFs) with or without GSK-3β inhibitor pretreatment. RESULTS Assessments of cardiac function, histochemical and biochemical assays for cardiac tissues, as well as detection of protein and m RNA expressions in heart tissues, showed that GSK-3β inhibition remarkably improves myocardial dysfunction and prevents remodeling with parallel reduction of the parameters of NLRP3 inflammasome activation after MI. The measurement of primary rats/human cells expounded that GSK-3β inhibition reduce NLRP3 inflammasome activation happens in cardiac fibroblasts, but not in cardiomyocytes. Futhermore, GSK-3β interacts with ASC and GSK-3β inhibition reduces cytoplasmic aggregates of ASC, NLRP3 and caspase-1 formation. CONCLUSION GSK-3β directly mediates NLRP3 inflammasome activation causing cardiac dysfunction in MI.

关键词： myocardial infarction glycogen synthase kinase 3 cardiac fibroblasts NLRP3 inflammasome ASC

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Effect of Lithium on Cell Cycle Progression of Pig Airway Epithelial Cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第4期24卷 318-321页

作者：陈文书吴人亮王曦李媛郝天玲 Department of Pathology Tongji Medical College Huazhong University of Science and Technology and Pulmonary Disease Laboratory Ministry of Health of China

To investigate the effect of lithium on cell cycle progression of airway epithelial cells, primary pig tracheobronchial epithelial cells were incubated with lithium chloride (LiCl) at different concentrations (0, 5 mmol/L, and 10 mmol/L) and time (12 h, 16 h and 24 h). After the treatment, cells were counted, cell cycle profile was measured by BrdU labeling and flow cytometry, and expression of cyclin D1 and cyclin B1 were detected by Western blotting. The results showed that after 24h of 10mmol/L but not 5mmol/L LiCl treatment, proliferation of cells was slowed down as manifested by delayed confluence and cell number accumulation (P0.05), but 24 h incubation with 10 mmol/L LiCl induced a G 2/M cell cycle arrest. Furthermore, 10mmol/L LiCl elevated cyclin D1 expression after 12h treatment, while expression of cyclin B1 increased more significantly after 24h incubation. These data demonstrate that lithium inhibits proliferation of pig airway epithelial cells by inhibiting cell cycle progression, and suggest that lithium-sensitive molecule(s) such as glycogen synthase kinase 3 may have a role in the regulation of growth of airway epithelial cells.

关键词： lithium airway epithelial cell cell cycle glycogen synthase kinase 3

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Inhibition of GSK-3β ameliorates hepatic ischemia-reperfusion injury through GSK-3β/ β-catenin signaling pathway in mice

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Hepatobiliary & Pancreatic Diseases International 2012年第3期11卷 278-284页

作者： Yong-Xiang Xia, Ling Lu, Zheng-Shan Wu, Li-Yong Pu, Bei-Cheng Sun and Xue-Hao Wang Liver Transplantation Center, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China Liver Transplantation Center First Affiliated Hospital Nanjing Medical University Nanjing 210029 China

BACKGROUND: glycogen synthase kinase (GSK)-3β/β-catenin signaling regulates ischemia-reperfusion (I/R)-induced apoptosis and proliferation, and inhibition of GSK-3β has beneficial effects on I/R injury in the heart and the central nervous system. However, the role of this signaling in hepatic I/R injury remains unclear. The present study aimed to investigate the effects and mechanism of GSK-3β/β-catenin signaling in hepatic I/R injury. METHODS: Male C57BL/6 mice (weighing 22-25 g) were pretreated with either SB216763, an inhibitor of GSK-3β, or vehicle. These mice were subjected to partial hepatic I/R. Blood was collected for test of alanine aminotransferase (ALT), and liver specimen for assays of phosphorylation at the Ser9 residue of GSK-3β, GSK-3β activity, axin 2 and the anti- apoptotic factors Bcl-2 and survivin, as well as the proliferative factors cyclin D1 and proliferating cell nuclear antigen, and apoptotic index (TUNEL). Real-time PCR, Western blotting and immunohistochemical staining were used. RESULTS: SB216763 increased phospho-GSK-3β levels and suppressed GSK-3β activity (1880±229 vs 3280±272 cpm, P3 decreased ALT after 6 hours of reperfusion (4451±424 vs 7868±845 IU/L, P3β inhibition led to the accumulation of β-catenin in the cytosol (0.40±0.05 vs 1.31±0.11, P3±0.12, P3β/β-catenin signaling increased Bcl-2, survivin and cyclin D1. Serological and histological analyses showed thatSB216763 alleviated hepatic I/R-induced injury by reducing apoptosis (1.4±0.2% vs 3.6±0.4%, P3β ameliorates hepatic I/R injury through the GSK-3β/β-catenin signaling pathway.

关键词： glycogen synthase kinase 3 beta-catenin reperfusion injury signal transduction

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Phosphoprotein Phosphatase 1 Isoforms Alpha and Gamma Respond Differently to Prodigiosin Treatment and Present Alternative kinase Targets in Melanoma Cells

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Journal of Biophysical Chemistry 2014年第2期5卷 67-77页

作者： Margarida Fardilha Joao Figueiredo Margarita Espona-Fiedler Juliana Felgueiras Luis Korrodi-Gregorio Sara L.C.Esteves Sandra Rebelo Odete A.B.da Cruz Silva Edgar da Cruz e Silva Ricardo Perez-Tomas Laboratory of Signal Transduction Centre for Cell BiologyBiology Department and Health Sciences DepartmentUniversity of AveiroAveiroPortugal Department of Pathology and Experimental Therapeutics Cancer Cell Biology Research GroupUniversity of BarcelonaBarcelonaSpain Laboratory of Neuroscience Centre for Cell BiologyBiology Department and Health Sciences DepartmentUniversity of AveiroAveiroPortugal

Reversible protein phosphorylation is a central regulatory mechanism of cell function. Deregulation of the balanced actions of protein kinases and phosphatases has been frequently associated with several pathological conditions, including cancer. Many studies have already addressed the role of protein kinases misregulation in cancer. However, much less is known about protein phosphatases influence. Phosphoprotein Phosphatase 1 (PPP1) is one of the major serine/threonine protein phosphatases who has three catalytic isoforms: PPP1CA, PPP1CB, and PPP1CC. Its function is achieved by binding to regulatory subunits, known as PPP1-interacting proteins (PIPs), which may prefer a catalytic isoform. Also, some inhibitors/enhancers may exhibit isoform specificity. Here we show that, prodigiosin (PG), a molecule with anticancer properties, promotes the formation of PPP1CA-AKT complex and not of PPP1CC-MAPK complex. Both, AKT and MAPK, are well-known PIPs from two pathways that crosstalk and regulate melanoma cells survival. In addition, the analysis performed using surface plasmon resonance (SPR) technology indicates that PPP1 interacts with obatoclax (OBX), a drug that belongs to the same family of PG. Overall, these results suggest that PG might, at least in part, act through PPP1C/PIPs. Also, this study is pioneer in demonstrating PPP1 isoform-specific modulation by small molecules.

关键词： Phosphoprotein Phosphatase 1 Catalytic Subunit Surface Plasmon Resonance Mitogen-Activated Protein kinase V-Akt Murine Thymoma Viral Oncogene glycogen synthase kinase 3

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Suppression of PTEN expression attenuates tau hyperphosphorylation by Akt/GSK-3 signaling

Suppression of PTEN expression attenuates tau hyperphosphory...

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中国药理学会第十一次全国学术会议

作者： CHEN Zhou,CHEN Bin,YANG Jian,XU Wen-fang,LIU Rong-fang,YU Chang-xi (Department of Pharmacology,College of Pharmacy,Fujian Medical University,Fuzhou 350004,China)

One of pathological hallmarks of Alzheimer’s disease(AD) is neurofibrillary tangles(NFTs) consisting of abnormally hyperphosphorylated *** molecular mechanisms underlying the regulation of tau hyperphosphorylation remain largely unclear. While the phosphoinositide 3-kinase(PI3K)/Akt pathway has been implicated in the pathogenesis of AD,potential functions and role of tumor suppressor phosphatase and tensin homologue deleted on chromosome 10(PTEN) in AD pathogenesis have not been fully explored. Here,we report that okadaic acid(OA)-induced tau phosphorylation is accompanied by PTEN induction,constitutive knock-down of PTEN reduces the tau hyperphosphorylation by OA in SH-SY5Y cells and increases cell proliferation and *** effect of PTEN downregulation on tau dephosphorylation appeared to be mediated by inhibition of glycogen synthase kinase-3 while enhancing the Akt *** studies provide evidence for an effect of PTEN on the phosphorylation of tau in AD pathogenesis,and provide some insight into the mechanisms through which down-regulation of PTEN may contribute towards the amelioration of tauopathy.

关键词： PTEN Akt/PKB glycogen synthase kinase 3 Alzheimer’s disease Tau phosphorylation

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