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Antioxidant Effects of Dehydroepiandrosterone Are Related to Up-regulation of Thioredoxin in sh-sy5y cells

Acta Biochimica et Biophysica Sinica 2005年第2期37卷 119-125页

作者： Jing GAO Hui-ying SUN Zeng-Rong ZHU Zhen DING Li ZHU School of Medicine.School of Life Sciences,Nanjing University.Nanjing 210093.China Institute of Nautical Medicine,Nantong University.Nantong 226001,China School of Medicine School of Life Sciences Nanjing UniversityNanjing 210093 China Institute of Nautical Medicine Nantong UniversityNantong 226001 China

Neuroprotective effects of dehydroepiandrosterone（DHEA）have been shown to be associatedwith its antioxidant properties,but the mechanisms remain unknown.Considering that the thioredoxin（Trx）system,an important cellular redox modulation system,changes under oxidative stress and could exertprotective effects,the relationship between the antioxidant effects of DHEA and the Trx system regulationwas explored.Using MTT assay and morphological observation,the effects of DHEA in the model of H2O2-induced oxidative stress in sh-sy5y cells were analyzed,then RT-PCR and Western blot assay were used todetect the alteration in mRNA and protein level of Trx,The results showed that a pre-treatment of DHEA（10-100nM）protected cells against the toxicity induced by H2O2in a dose-dependent manner,which could beconfirmed in morphological observation by phase-contract microscope.In addition,Trx mRNA transcriptionwas inhibited by H2O2（300μM）,which could be reversed by the pre-administration of DHEA in variousconcentrations（0.1-100nM）.Western blot assay confirmed that protein level of Trx could be elevated by thepre-treatment of DHEA（10-100nM）with the exposure of H2O2.Taken together,these data suggest thatDHEA may be useful in treating age-related neurodegenerative diseases based on its up-regulating effects onan antioxidant and neuroprotective protein thioredoxin,a substrate in the Trx redox system.

关键词： dehydroepiandrosterone(DHEA) thioredoxin(Trx) H2O2 sh-sy5y cell

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Nanomolar concentration of alpha-synuclein enhances dopaminergic neuronal survival via Akt pathway

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Neural Regeneration Research 2013年第35期8卷 3269-3274页

作者： Ji-young Kim Beom Seok Jeon Han-Joon Kim Tae-Beom Ahn Department of Neurology Inje University Seoul Paik Hospital Department of Neurology College of Medicine Seoul National University Hospital Department of Neurology Kyung Hee University Medical Center

Although alpha-synuclein is generally thought to have a pathological role in Parkinson＇s disease, accumulative evidence exists that alpha-synuclein has a neuroprotective effect. The aim of this study was to evaluate the effect of extracellular alpha-synuclein on dopaminergic cell survival. We assessed cell viability using the 3-（4,5-dimethyt-thiazol-2-yt）-2,5-diphenyltertazolium bromide （MTT） assay both in undifferentiated sh-sy5y （shsy） cells and neuronally-differentiated sh-sy5y （ndshsy） cells after 24 hour treatment with monomeric alpha-synuclein at various concentrations （0 [control], 50, 100 nmol/L, 1 IJmol/L）. To determine whether cell viability assessed by MTT assay was affected by cell proliferation, 5-bromo-2＇-deoxyuridine （BrdU） incorporation assay was per- formed. Level of both Akt and phosphorylated Akt was measured using western blot method in ndshsy cells with or without 24 hour alpha-synuclein treatment. cell viability was increased in ndshsy cells at the nanomolar concentration of alpha-synuclein, but not in shsy cells. Proportion of BrdU-positive ndshsy cells was decreased in alpha-synuclein-treated group compared with control group. Level of phosphorylated Akt in alpha-synuclein-treated group was higher compared with the control group. Our study shows that extracellular alpha-synuclein at nanomolar concentra- tion benefits dopaminergic cell survival via Akt pathway.

关键词： neural regeneration alpha-synuclein neuronal survival nanomolar extracellular phosphorylatedAkt sh-sy5y cell neuronal differentiation proliferation dopaminergic 5-bromo-2＇-deoxyuridine grants-supported paper neuroregeneration

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DADLE对sh-sy5y细胞缺氧复氧损伤的保护作用

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解剖学杂志 2020年第1期43卷 31-36页

作者：刘麟文周雅春姚俊岩上海交通大学医学院附属第一人民医院麻醉科

目的:探讨[D-Ala2,D-Leu5]enkephalin(DADLE)对人神经母细胞瘤细胞sh-sy5y细胞的缺氧复氧的保护作用。方法:将体外培养的sh-sy5y细胞分别缺氧6、12、24 h和48 h,均复氧4 h后观察细胞形态改变,采用MTT法检测细胞生存率,评估细胞损伤程度... 详细信息

目的:探讨[D-Ala2,D-Leu5]enkephalin(DADLE)对人神经母细胞瘤细胞sh-sy5y细胞的缺氧复氧的保护作用。方法:将体外培养的sh-sy5y细胞分别缺氧6、12、24 h和48 h,均复氧4 h后观察细胞形态改变,采用MTT法检测细胞生存率,评估细胞损伤程度。在此基础上,于缺氧12 h期间首先给予DADLE 100 pmol/L作用于细胞,评价DADLE能否减轻神经细胞缺氧复氧损伤;继而分别用10 pmol/L、100 pmol/L、1 nmol/L、10 nmol/L和100 nmol/L不同浓度的DADLE溶液处理细胞,研究DADLE保护作用是否具有剂量效应关系。结果:sh-sy5y细胞缺氧6、12、24 h或48 h,复氧4 h后,细胞生存率分别为(68.1±4.3)%、(52.6±2.8)%、(26.7±1.5)%或(3.5±1.7)%。sh-sy5y细胞缺氧12 h期间给予DADLE 100 pmol/L处理可使细胞生存率上升到(58.7±0.46)%。5个给药浓度中,10 pmol/L和100 pmol/L DADLE可使神经细胞生存率上升,而1、10 nmol/L和100 nmol/L则变化不明显。结论:DADLE对sh-sy5y的缺氧复氧损伤具有保护作用,且其保护效果呈现出较小剂量优于较大剂量的量效关系,本实验中最佳保护剂量为10 pmol/L。

关键词： DADLE 缺氧复氧神经保护 sh-sy5y cell

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Neuroprotective effects of asiatic acid against Parkinson-like injury of sh-sy5y cells and motor deficient of mutant drosophilas

Neuroprotective effects of asiatic acid against Parkinson-li...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： yu-yun XIONG~1,Hong-Qun DING~2,Min-Fang XU~1,Jing GAO~(1,*) 1 School of Pharmacy 2 School of Medicine,Jiangsu University,Zhenjiang,212013,China

Parkinson’s disease(PD) is a progressive neurodegenerative disorder with a prevalence of l%-2%in people over the age of 50.oc-synuclein is a major protein component of Lewy bodies and Lewy neuritis that are involved in the pathology of PD.Overexpression ofα-synuclein in cells has been suggested to cause elevation of mitochondrial oxidant radicals and mitochondrial structural and functional abnormalities.Pathogenesis of PD mainly includes oxidative stress, mitochondrial dysfunction,excitotoxicity,calcium overloading,trophic factor deficiency,inflammatory processes,and also genetic factor.Increasing evidence suggests that both oxidative stress and mitochondrial dysfunction,which interact and amplify each other in a vicious cycle of toxicity,lead to neuronal dysfunction and finally cell death.Asiatic acid(AA), a triterpenoid,is an antioxidant and used for depression treatment,but the effect of AA against PD-like damage has never been reported.In the present study,the effects of improving motor dysfunction and lifespan were studied in an ocsynuclein transgenic Drosophila Parkinson’s model.And then the effects of AA against rotenone,HO or glutamate acid (Glu)-induced cellular injury and mitochondrial dysfunction in sh-sy5y cells were investigated using MTT assay.ROS generation,mitochondrial membrane potential(MMP) and the expression of voltage-dependent anion channel(VDAC) were detected with or without AA pretreatment following cellular injury to address the possible mechanisms of AA neuroprotection.Finally,Glu-induced mitochondrial swelling was analyzed to show the direct effect of AA on mitochondria. The results showed that in the drosophila model,AA at 1 mg/100 g diet can significantly improve climbing ability and extended life-span.And both treatment and pre-treatment of AA(0.01-100 nmol/L) protected cells against the toxicity induced by rotenone,HO or Glu.In addition,0.1-10 nmol/L AA can scavenge ROS induced by Glu.MMP dissipation following the exposure of rotenone could be blocked by AA treatment.More interestin

关键词： Parkinson’s disease mitochondrion asiatic acid α-synuclein sh-sy5y cell transgenic Drosophila

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Drug repurposing identifies econazole as a novel neuroprotective agent that activates autophagy/mitophagy in Parkinson disease models

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中国药理学与毒理学杂志 2019年第10期 780-780页

作者： ZHEN yong-qi ZHAO yu-qian FU Lei-lei LIU Bo School of Life Science and Engineering Southwest Jiaotong University State Key Laboratory of Biotherapy and Cancer Center West China Hospital Sichuan University

OBJECTIVE To discover new drugs for Parkinson disease(PD), we sought to focus on its pathogenesis. Autophagy is involved in the pathogenesis of PD, and recent accumulating evidence has revealed that defects in autophagy have implications for potential therapy.To our knowledge, PD treatment with conventional drugs may result in some serious adverse reactions; therefore,discovery of more autophagic inducers will be a possible strategy. METHODS The mechanisms of econazole induced cytoprotective autophagy were investigated by electron microscopy, fluorescence microscopy, Western blotting, co-immunoprecipitation assay, si RNA and GFP-LC3 plasmid transfections. The therapeutic effect of econazole was determined by MPTP-mouse model, including behavioral tests, the levels of dopamine and its derivatives, as well as immunofluorescence and Western blotting. RESULTS Econazole could trigger autophagy by the ULK complex and ATG5-dependent pathways in sh-sy5 y cells. Econazole was also found to induce mitophagy via the activation of Parkin-PINK1 pathway.Interestingly, econazole had a cytoprotective autophagic effect by ameliorating MPP+-induced cell death as well as reducing expression of α-synuclein inα-synu A53 T sh-sy5 y cells. Moreover, we demonstrated that econazole had a neuroprotective effect on mouse and zebrafish models of PD, respectively. Combined with microarray analyses of mouse brain tissues, econazole could inhibit apoptosis by DLK-JNK pathway, and activated autophagy by Ambra1-Beclin1-Vps34 complex. CONCLUSION Econazole, an old anti-fungal drug, would be utilized as a novel neuroprotective agent that activates autophagy/mitophagy for the future PD therapeutics.

关键词： autophagy Parkinson disease econazole ULK complex mitophagy sh-sy5y cell α-synuclein

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