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glycogen synthase kinase-3β positively regulates the proliferation of human ovarian cancer cells

Cell Research 2006年第7期16卷 671-677页

作者： Qi Cao~1 Xin Lu~1 You-Ji Feng ~1Department of Gynecology,Obstetrics and Gynecology Hospital,Fudan University,Shanghai 200011,China DepartmentofGynecology ObstetricsandGynecologyHospitalFudanUniversityShanghai200011China

Although glycogen synthase kinase-3(GSK-3)might act as a tumor suppressor since its inhibition is expected tomimic the activation of Wnt-signaling pathway,GSK-3β may contribute to NF-κ3 activation in cancer cells leading toincreased cancer cell proliferation and *** we report that GSK-3β activity was involved in the proliferationof human ovarian cancer cell both in vitro and in *** of GSK-3 activity by pharmacological inhibitors sup-pressed proliferation of the ovarian cancer *** constitutively active form of GSK-3β induced entryinto the S phase,increased cyclin D1 expression and facilitated the proliferation of ovarian cancer ***,GSK-3 inhibition prevented the formation of the tumor in nude mice generated by the inoculation of human ovariancancer *** findings thus suggest that GSK-3β activity is important for the proliferation of ovarian cancer cells,implicating this kinase as a potential therapeutic target in ovarian cancer.

关键词： glycogen synthase kinase 3β ovarian cancer cell proliferation therapeutic target

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Overexpression of fibroblast growth factor 13 ameliorates amyloid-β-induced neuronal damage

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Neural Regeneration Research 2023年第6期18卷 1347-1353页

作者： Ruo-Meng Li Lan Xiao Ting Zhang Dan Ren Hong Zhu Department of Traditional Chinese Medicine The Third Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina

Previous studies have shown that fibroblast growth factor 13 is downregulated in the brain of both Alzheimer’s disease mouse models and patients,and that it plays a vital role in the learning and ***,the underlying mechanisms of fibroblast growth factor 13 in Alzheimer’s disease remain *** this study,we established rat models of Alzheimer’s disease by stereotaxic injection of amyloid-β(Aβ_(1-42))-induced into bilateral *** also injected lentivirus containing fibroblast growth factor 13 into bilateral hippocampus to overexpress fibroblast growth factor *** expression of fibroblast growth factor 13 was downregulated in the brain of the Alzheimer’s disease model *** overexpression of fibroblast growth factor 13,learning and memory abilities of the Alzheimer’s disease model rats were remarkably *** growth factor 13 overexpression increased brain expression levels of oxidative stress-related markers glutathione,superoxide dismutase,phosphatidylinositol-3-kinase,AKT and glycogen synthase kinase 3β,and anti-apoptotic factor ***,fibroblast growth factor 13 overexpression decreased the number of apoptotic cells,expression of pro-apoptotic factor BAX,cleaved-caspase 3 and amyloid-βexpression,and levels of tau phosphorylation,malondialdehyde,reactive oxygen species and acetylcholinesterase in the brain of Alzheimer’s disease model *** changes were reversed by the phosphatidylinositol-3-kinase inhibitor *** findings suggest that overexpression of fibroblast growth factor 13 improved neuronal damage in a rat model of Alzheimer’s disease through activation of the phosphatidylinositol-3-kinase/AKT/glycogen synthase kinase 3βsignaling pathway.

关键词： AKT Alzheimer’s disease amyloid-β apoptosis cognitive dysfunction fibroblast growth factor 13 glycogen synthase kinase 3β neuronal damage oxidative stress phosphatidylinositol-3-kinase

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1,5-dicaffeoylquinic acid protects primary neurons from amyloid β1-42-induced apoptosis via PI3K/Akt signaling pathway

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Chinese Medical Journal 2011年第17期124卷 2628-2635页

作者： XIAO Hai-bing CAO Xu WANG Lei RUN Xiao-qin SU Ying TIAN Cheng SUN Sheng-gang LIANG Zhi-hou Department of Neurology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430022 China Department of Neurology Shenzhen People's Hospital Jinan University Shenzhen Guangdong 518020 China Department of Vascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430022 China Department of Neurology Shenzhen Sixth People's Hospital (Nanshan Hospital) Shenzhen Guangdong 518052 China

Background Recently, 1,5-dicaffeoylquinic acid （1,5-DQA）, a caffeoylquinic acid derivative isolated from Aster scaber, was found to have neuroprotective effects. However, the protective mechanisms of 1,5-DQA have not yet been clearly identified. The purpose of this study was to explore the protective mechanisms of 1,5-DQA on neuronal culture. Methods We investigated the neuroprotective effects of 1,5-DQA against amyloid IB1-42 （Aβ42）-induced neurotoxicity in primary neuronal culture. To evaluate the neuroprotective effects of 1,5-DQA, primary cultured cortical neurons from neonate rats were pretreated with 1,5-DQA for 2 hours and then treated with 40 pmol/L Aβ42 for 6 hours. Cell counting kit-8, Hoechst staining and Western blotting were used for detecting the protective mechanism. Comparisons between two groups were evaluated by independent t test, and multiple comparisons were analyzed by one-way analysis of variance （ANOVA）. Results 1,5-DQA treated neurons showed increased neuronal cell viability against Aβ42 toxicity in a concentration- dependent manner, both phosphoinositide 3-kinase （PI3K）/Akt and extracellular regulated protein kinase 1/2 （Erkl/2） were activated by 1,5-DQA with stimulating their upstream tyrosine kinase A （Trk A）. However, the neuroprotective effects of 1,5-DQA were blocked by LY294002, a PI3K inhibitor, but not by PD98059, an inhibitor of mitogen-activated protein kinase kinase. Furthermore, 1,5-DQA＇s anti-apoptotic potential was related to the enhanced inactivating phosphorylation of glycogen synthase kinase 313 （GSK3β） and the modulation of expression of apoptosis-related protein Bcl-2/Bax. Conclusion These resutts suggest that 1,5-DQA prevents AI342-induced neurotoxicity through the activation of PI3K/Akt followed by the stimulation of Trk A, then the inhibition of GSK313 as well as the modulation of Bcl-2/Bax.

关键词： Alzheimer's disease," amyloid beta-peptides 1,5-dicaffeoylquinic acid phosphoinositide 3-kinase glycogen synthase kinase 3β extracellular regulated protein kinase

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Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenic Drosophila model of Alzheimer’s disease

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Translational Neurodegeneration 2016年第1期5卷 165-170页

作者： Bei Zhang Qiongqiong Li Xingkun Chu Suya Sun Shengdi Chen Department of Neurology and Institute of Neurology Ruijin HospitalShanghai Jiao Tong University School of Medicine197 Ruijin Er RoadShanghai 200025China Laboratory of Neurodegenerative Diseases Institute of Health SciencesShanghai Institutes for Biological Sciences(SIBS)Chinese Academy of Sciences(CAS)&Shanghai Jiao Tong University School of Medicine(SJTUSM)Shanghai 200025China

Background:Alzheimer’s disease(AD)is an age-related and progressive neurodegenerative disease that causes substantial public health care *** efforts have been made to find effective and safe treatment against ***(Sal)is the main effective component of Rhodiola rosea L.,which has several pharmacological *** objective of this study was to investigate the efficacy of Sal in the treatment of AD transgenic Drosophila and the associated ***:We used tau transgenic Drosophila line(TAU)in which tau protein is expressed in the central nervous system and eyes by the Gal4/UAS *** feeding flies with Sal,the lifespan and locomotor activity were *** further examined the appearance of vacuoles in the mushroom body using immunohistochemistry,and detected the levels of total glycogen synthase kinase 3β(t-GSK-3β),phosphorylated GSK-3β(p-GSK-3β),t-tau and p-tau in the brain by western blot ***:Our results showed that the longevity was improved in salidroside-fed Drosophila groups as well as the locomotor *** also observed less vacuoles in the mushroom body,upregulated level of p-GSK-3βand downregulated p-tau following Sal ***:Our data presented the evidence that Sal was capable of reducing the neurodegeneration in tau transgenic Drosophila and inhibiting neuronal *** neuroprotective effects of Sal were associated with its up-regulation of the p-GSK-3βand down-regulation of the p-tau.

关键词： Alzheimer’s disease Salidroside Drosophila glycogen synthase kinase 3β Tau

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GSK3β inhibits epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt pathways

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International Journal of Ophthalmology(English edition) 2018年第7期11卷 1120-1128页

作者： Cheng Zhang Li Su Li Huang Zheng-Yu Song Department of Ophthalmology Shanghai General Hospital(Shanghai First People's Hospital) Shanghai Jiao Tong University School of Medicine Shanghai 200000 China Shanghai Key Laboratory of Fundus Diseases Shanghai 200000 China Shanghai Engineering Center for Visual Science and Photomedicine Shanghai 200000 China Department of Ophthalmology Shanghai Shuguang HospitalShanghai University of Traditional Chinese MedicineShanghai 200000 China

AIM： To investigate the regulatory mechanism of glycogen synthase kinase 3β（GSK3β） in epithelialmesenchymal transition（EMT） process after proliferative vitreoretinopathy（PVR） induction. METHODS： Experimental PVR was induced by intravitreal injection of retinal pigment epithelium（RPE） cells in the eyes of rabbits. A PI3 K/Akt inhibitor（wortmannin） and a GSK3β inhibitor（Li Cl） were also injected at different time during PVR progress. Electroretinogram（ERG）, ocular fundus photographs, and B-scan ultrasonography were used to observe the PVR progress. Western blot test on the extracted retina were performed at 1, 2, 4 wk. The expression of the mesenchymal marker vimentin was determined by immunohistochemistry. Toxicity of wortmannin and Li Cl were evaluated by ERG and Td Tmediated d UTP nick-end labeling（TUNEL） assay. The vitreous was also collected for metabolomic analysis. RESULTS： Experimental PVR could significantly lead to EMT, along with the suppressed expression of GSK3β and the activation of Wnt/β-catenin and PI3 K/Akt pathways. It was verified that upregulating the expression of GSK3β could effectively inhibit EMT process by suppressing Wnt/β-catenin and PI3 K/Akt pathways. CONCLUSION： GSK3β effectively inhibits EMT via the Wnt/β-catenin and PI3 K/Akt pathways. GSK3β may be regarded as a promising target of experimental PVR inhibition.

关键词： epithelial-mesenchymal transition experimental proliferative vitreoretinopathy glycogen synthase kinase 3β rabbits

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Cardioprotective mechanism of atrial natriuretic peptide

Cardioprotective mechanism of atrial natriuretic peptide

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2012年中美临床和转化医学国际论坛心脑血管病分会论坛...

作者： Lan Hong1,Zhengai Chen2,Xun Cui1 1 Department of Physiology,College of Medicine,Yanbian University,Yanji,China 2 Department of Pharmacology,College of Medicine,Yanbian University,Yanji,China.

＜正＞Heart is no longer considered only as an efficient pump but also as an important endocrine organ, becausre the heart generates and secretes atrial natriuretic peptide（ANP）.It is well known that ANP have important biological effects,such as diuresis and natriuresis,modulating blood pressure and cardiovascular homeostasis by combining with natriuretic peptide *** binds to NPR-A receptor which is a member of the membrane-bound guanylyl cyclase family and exerts its biological effects by increasing cGMP levels.

关键词： Atrial natriuretic peptide Mitochondrial permeability transition pore glycogen synthase kinase 3β Myocardial ischemia/reperfusion injury Protein kinase G Phosphoinositide 3-kinase/Akt

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The effects of antipsychotics on AKT/GSK3 signalling pathway:implications for treatment of memory impairment for schizophrenia

The effects of antipsychotics on AKT/GSK3 signalling pathway...

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中国神经科学学会第十届全国学术会议

作者： Mei HAN Chong-Sheng SONG Hong-Qin WANG Xu-Feng HUANG Center for Translational Neuroscience School of Health SciencesIHMRIUniversity of Wollongong Center for Biological Psychiatry Beijing HuiLongGuan HospitalPeking University

Objective Cognitive impairment is a core feature of *** impairment of AKT-glycogen synthase kinase 3p(GSK3β) signalling pathway in the hippocampus has been involved in memory impairment in schizophrenia and other schizophrenic *** evidence supports that antipsychotics may partly improve cognition such as memory function in patients with *** study is to investigate the effects of haloperidol and olanzapine in the AKT/GSK3B signalling pathway in the rat hippocampus and understand the possible pharmacological mechanisms of antipsychotics in improving cognitive *** Female rats were treated with haloperidol(0.1mg/kg),olanzapine(1.0mg/kg) or saline for one times,three times/day for 3 days and 6 *** were then sacrificed after two hours once the last injection was *** blotting was employed to determine total and phosphorylated protein levels of AKT and GSK 3β in the hippocampus of female *** analyses were used to detect any differences between treatment and *** Overall,compared to salines,haloperidol and olanzapine showed significant treatment effects on the levels of GSK3β total proteins and phosphorylation of AKT and GSK3β(all P3β total proteins and phosphorylation of GSK3β in the hippocampus after a single ***,olanzapine significantly increased expression levels in phosphorylation of GSK3β.At the three days time-points,haloperidol significantly increased phosphorylation of AKT3β and GSK3β(all P3β.Furthermore,both antipsychotics significantly increased phosphorylation of AKT and GSK3β at the six days ***,the total AKT protein levels were significant increased by haloperidol(P<0.05) and had been increased tread by olanzapine(P=0.061) at this *** These results suggested that antipsychotics

关键词： schizophrenia memory impairment glycogen synthase kinase 3β phosphorylation AKT

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Isoorientin inhibits LPS-induced neuroinflammation by regulating GSK3β pathway in microglia

Isoorientin inhibits LPS-induced neuroinflammation by regula...

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第十四届全国免疫学学术大会

作者： Yan Dong Xiaoqin Tan Mindie Cao Yijing Zhao Yingui Li Changhong He Lang Yi Qingxiao Li Guangzhou University of Chinese Medicine Department of Molecular Biosciences and Bioengineering University of Hawaii at Manoa

Background:Isoorientin(ISO),a Chinese herbal medicinal ingredient,has recently received attention due to its considerable promise in preventing and managing cancers,diabetes,and vascular inflammatory *** study found ISO isolated from corn silk could selectively inhibit glycogen synthase kinase 3β(GSK3β) via a substrate-competitive ***3β is considered to be a key component in many neuronal signaling *** studies suggest that the inhibition of GSK3β significantly inhibited neuroinflammation and improved neuron ***,as resident immune cells in the brain,is closely associated with ***:To investigate the neuroprotection of ISO by inhibiting neuroinflammation through regulating GSK3β pathway in microglia cells simulated by *** Mouse microglia SIM-A9 cells were used to construct an in vitro inflammation model stimulated by LPS(100 ng/mL).The effects of ISO(200μM) and LiCI(1 00μM) were *** is a GSK3β inhibitor as the positive *** release of TNF-α and NO were analyzed by ELISA and *** expressions of COX-2,BDNF,GSK3β,p-GSK3β-ser9,IκB and NF-κB p65,Nrf2 and HO-1 were detected by western *** the co-culture model of SIM-A9 cells and differentiated SHSY5 Y human neuroblastoma cells,MTS assay was used to evaluate the effect of ISO on LPS-induced microglia-mediated neuronal ***:ISO significantly inhibited the production of TNF-α,NO and COX-2 induced by *** increased the expression of BDNF,p-GSK3β-ser9,IκB,HO-1 and Nrf2 in the nucleus,decreased NF-κB p65 protein expression in the nucleus compared with LPS *** cell viability of SH-SY5 Y was inhibited by LPS in co-culture,but not in SH-SY5 Y *** cell viability of SH-SY5 Y in co-culture was increased by ISO ***:ISO attenuated LPS-induced microglia activation through regulating the GSK3β/NF-κB and GSK3β/N rf2/HO-1 signaling pathways to exert neuroprotection.

关键词： isoorientin glycogen synthase kinase 3β neuroinflammation microglia

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