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Artemisinin protected human sy5Y and hippocampal neurons from H2O2-induced oxidative damage through activation of AMPK pathway

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中国药理学与毒理学杂志 2018年第9期32卷 703-704页

作者： JIANG Yi-zhou ZHAO Xia ZHENG wen-hua Faculty of Health Sciences University of Macao Taipa China

Oxidative stress is one of the main causes of neurodegenerative diseases such as Alzheimer disease(AD).Our previous studies have shown that artemisinin,a anti-malaria Chinese medicine,with neuroprotective effect,however,the antioxidative effect of artemisinin and its potential mechanism remain to be *** the present study,the protective effect and the underlying mechanism of artemisinin against injury of hydrogen peroxide(H_2O_2) in SH-sy5Y and hippocampal neurons were *** results show that artemisinin protected SH-sy5Y and hippocampal neuronal cells from H_2O_2-induced cell death at clinically relevant concentrations in a concentration-dependent *** studies showed that artemisinin significantly reduced cell death caused by H_2O_2 by restoring nuclear morphology,abnormal changes in intracellular ROS,activation of caspase 3,lactate dehydrogenase release and mitochondrial membrane *** staining and flow cytometry showed that artemisinin significantly reduced the apoptosis of SH-sy5Y cells exposed to H_2O_*** blotting analysis showed that artemisinin stimulated the phosphorylation and activation of AMP-activated protein kinase(AMPK) in SH-sy5Y cells in a time and concentration-dependent manner,whereas the application of AMPK inhibitor Compound C or decrease in expression of AMPKα with shRNA specific for AMPKα blocked the protective effect of *** results were obtained in primary cultured hippocampal *** together,these results indicate that artemisinin can protect neuronal cells from oxidative damage,at least in part through the activation of *** artemisinin is relatively inexpensive and has few side effects,our findings support the role of artemisinin as a potential therapeutic agent for neurodegenerative diseases.

关键词： artemisinin hydrogen peroxide SHsy5Y cells hippocampal neurons AMPK pathway

Suppressing high mobility group box-1 release alleviates morphine tolerance via the adenosine5'-monophosphate-activated protein kinase/heme oxygenase-1 pathway

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Neural Regeneration Research 2023年第9期18卷 2067-2074页

作者： Tong-Tong Lin Chun-Yi Jiang Lei Sheng Li Wan wen Fan Jin-Can Li Xiao-Di Sun Chen-Jie Xu Liang Hu Xue-Feng Wu Yuan Han wen-Tao Liu Yin-Bing Pan Jiangsu Key Laboratory of Neurodegeneration Department of PharmacologyNanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Anesthesiology The First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Anesthesiology and Pain Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina State Key Laboratory of Pharmaceutical Biotechnology Nanjing UniversityNanjingJiangsu ProvinceChina Department of Anesthesiology Eye&ENT HospitalFudan UniversityShanghaiChina Institute of Translational Medicine Nanjing Medical UniversityNanjingJiangsu ProvinceChina

Opioids,such as morphine,are the most potent drugs used to treat ***-term use results in high tolerance to *** mobility group box-1(HMGB1) has been shown to participate in neuropathic or inflammatory pain,but its role in morphine tolerance is *** this study,we established rat and mouse models of morphine tolerance by intrathecal injection of morphine for 7 consecutive *** found that morphine induced rat spinal cord neurons to release a large amount of ***1 regulated nuclear factor κB p65 phosphorylation and interleukin-1β production by increasing Toll-like receptor 4receptor expression in microglia,thereby inducing morphine ***,an HMGB1 inhibito r,markedly attenuated chronic morphine tole rance in the mouse ***,compound C(adenosine 5’-monophosphate-activated protein kinase inhibitor) and zinc protoporphyrin(heme oxygenase-1 inhibitor)alleviated the morphine-induced release of HMGB1 and reduced nuclear factor κB p65 phosphorylation and interleukin-1β production in a mouse model of morphine tolerance and an SH-sy5Y cell model of morphine tole rance,and alleviated morphine tolerance in the mouse *** findings suggest that morphine induces HMGB1 release via the adenosine 5’-monophosphate-activated protein kinase/heme oxygenase-1 signaling pathway,and that inhibiting this signaling pathway can effectively reduce morphine tole rance.

关键词： adenosine 5’-monophosphate-activated protein kinase heme oxygenase-1 high mobility group box-1 interleukin-1β microglia morphine tolerance neuroinflammation neuron nuclear factor-κB p65 Toll-like receptor 4

Neuroprotective effect of deferoxamine on erastin-induced ferroptosis in primary cortical neurons

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Neural Regeneration Research 2020年第8期15卷 1539-1545页

作者： Yan Zhang Bao-You Fan Yi-Lin Pang wen-Yuan Shen Xu Wang Chen-Xi Zhao wen-Xiang Li Chang Liu Xiao-Hong Kong Guang-Zhi Ning Shi-Qing Feng Xue Yao Department of Orthopedics General Hospital of Tianjin Medical UniversityTianjinChina International Science and Technology Cooperation Base of Spinal Cord Injury Tianjin Key Laboratory of Spine and Spinal Cord InjuryTianjinChina Laboratory of Medical Molecular Virology School of MedicineNankai UniversityTianjinChina

The iron chelator deferoxamine has been shown to inhibit ferroptosis in spinal cord ***,it is unclear whether deferoxamine directly protects neurons from ferroptotic cell *** comparing the survival rate and morphology of primary neurons and SH-sy5Y cells exposed to erastin,it was found that these cell types respond differentially to the duration and concentration of erastin ***,we studied the mechanisms of ferroptosis using primary cortical neurons from E16 mouse *** treatment with 50μM erastin for 48 hours,reactive oxygen species levels increased,and the expression of the cystine/glutamate antiporter system light chain and glutathione peroxidase 4 *** with deferoxamine for 12 hours inhibited these changes,reduced cell death,and ameliorated cellular *** with the apoptosis inhibitor Z-DEVD-FMK or the necroptosis inhibitor necrostain-1 for 12 hours did not protect against erastin-induced *** deferoxamine protected the primary cortical neurons from ferroptosis induced by erastin,confirming the specificity of the in vitro ferroptosis *** study was approved by the Animal Ethics Committee at the Institute of Radiation Medicine of the Chinese Academy of Medical Sciences,China(approval ***-20180913)on September 13,2018.

关键词： cystine/glutamate antiporter system light chain deferoxamine erastin ferroptosis glutathione peroxidase 4 neurons neuroprotection reactive oxygen species

Action of trichostatin A on Alzheimer’s disease-like pathological changes in SH-sy5Y neuroblastoma cells

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Neural Regeneration Research 2020年第2期15卷 293-301页

作者： Li-Hua Li wen-Na Peng Yu Deng1 Jing-Jing Li Xiang-Rong Tian College of Medicine Jishou UniversityJishouHunan ProvinceChina Department of Rehabilitation Second Xiangya HospitalChangshaHunan ProvinceChina College of Biology and Environmental Science Jishou UniversityJishouHunan ProvinceChina

The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the nuclear factor erythroid 2-related factor 2(Nrf2) and Kelch-like epichlorohydrin-related protein-1(Keap1) signaling pathway, amyloid β-peptide 25–35(Aβ25–35) was used to induce Alzheimer’s disease-like pathological changes in SH-sy5 Y neuroblastoma cells. Cells were then treated with trichostatin A. The effects of trichostatin A on the expression of Keap1 and Nrf2 were detected by real-time quantitative polymerase chain reaction, western blot assays and immunofluorescence. Total antioxidant capacity and autophagy activity were evaluated by total antioxidant capacity assay kit and light chain 3-I/II levels, respectively. We found that trichostatin A increased cell viability and Nrf2 expression, and decreased Keap1 expression in SH-sy5 Y cells. Furthermore, trichostatin A increased the expression of Nrf2-related target genes, such as superoxide dismutase, NAD(P)H quinone dehydrogenase 1 and glutathione S-transferase, thereby increasing the total antioxidant capacity of SH-sy5 Y cells and inhibiting amyloid β-peptide-induced autophagy. Knockdown of Keap1 in SH-sy5 Y cells further increased trichostatin A-induced Nrf2 expression. These results indicate that the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the Keap1-Nrf2 pathway. The mechanism for this action may be that trichostatin A increases cell viability and the antioxidant capacity of SH-sy5 Y cells by alleviating Keap1-mediated inhibition Nrf2 signaling, thereby alleviating amyloid β-peptide-induced cell damage.

关键词： Alzheimer's disease amyloid-β peptide autophagy Keap1 signal neurocytotoxicity oxidative stress damage SH-sy5Y cells total antioxidant capacity transcription factor Nrf2 TSA

Relativistic Mean Field Study of the Z -- 117 Isotopic Chain

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Chinese Physics Letters 2010年第6期27卷 52-55页

作者： GAO Yuan ZHANG Hong-Fei ZHANG Lei CHEN Xi-Meng LI Jun-Qing GUO wen-Jun School of Information Engineering Hangzhou Dianzi University Hangzhou 310018 School of Nuclear Science and Technology Lanzhou University Lanzhou 730000 Institute of Modern Physics Chinese Academy of Sciences Lanzhou 730000 College of Science University of Shanghai for Science and Technology Shanghai 200093

The properties of the Z = 117 isotopic chain are studied within the framework of the axially deformed relativistic mean field theory （RMFT） in the blocked BCS approximation. The ground-state properties, such as hinging energies, deformations as well as the possible α decay energies and lifetimes are calculated with the parameter set of NL-Z2 and compared with results from the finite range droplet model. The analysis by RMFT shows that the isotopes in the range of mass number A =291 ~ 300 exhibit higher stability, which suggests that they may be promising nuclei to be hopefully synthesized in the lab among the nuclei Z = 117.

关键词： Property Properties Isotopes Energy

T-type calcium channel expression in cultured human neuroblastoma cells

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Neural Regeneration Research 2011年第31期6卷 2410-2413页

作者： Xianjie wen Shiyuan Xu Lingling Wang Hua Liang Chengxiang Yang Hanbing Wang Hongzhen Liu Department of Anesthesiology Zhujiang Hospital of Southern Medical University Guangzhou 510282 Guangdong Province China Department of Anesthesiology Foshan Hospital of Sun Yat-sen University ＆ First People＇s Hospital of Foshan Foshan 528000 Guangdong Province China

Human neuroblastoma cells （SH-sy5Y） have similar structures and functions as neural cells and have been frequently used for cell culture studies of neural cell *** studies have revealed L-and N-type calcium channels in SH-sy5Y ***,the distribution of the low-voltage activated calcium channel （namely called T-type calcium channel,including Cav3.1,Cav3.2,and Cav3.3） in SH-sy5Y cells remains poorly *** present study detected mRNA and protein expres-sion of the T-type calcium channel （Cav3.1,Cav3.2,and Cav3.3） in cultured SH-sy5Y cells using real-time polymerase chain reaction （PCR） and western blot *** revealed mRNA and protein expression from all three T-type calcium channel subtypes in SH-sy5Y ***,Cav3.1 was the predominant T-type calcium channel subtype in SH-sy5Y cells.

关键词： calcium ion channel calcium signaling cell culture neural regeneration real-time PCR T-type calcium channel western blot neural regeneration

Inhibition of high-mobility group box 1 expression by siRNA in rat hepatic stellate cells

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World Journal of Gastroenterology 2011年第36期17卷 4090-4098页

作者： wen-Song Ge Jian-Xin Wu Jian-Gao Fan Ying-Wei Chen Yao-Jun Wang Department of Gastroenterology Shanghai Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200092China Department of Gastroenterology General Hospital of Jinan Military RegionJinan 250031Shandong ProvinceChina

AIM:To explore the role of high-mobility group box 1 (HMGB1) protein during liver fibrogenesis and investigate the functional effects of HMGB1 gene silencing in hepatic stellate cells (HSCs) using ***:Hepatic fibrosis in rats was induced through serial subcutaneous injections of dimethylnitrosamine,and expression of HMGB1 was detected by ***1 siRNAs were developed and transiently transfected into HSC-T6 cells using Lipofectamine ***1 expression was evaluated by real-time polymerase chain reaction (PCR) and Western blotting *** of α-smooth muscle actin (α-SMA) and collagen typesⅠand Ⅲ was evaluated by real-time *** proliferation and the cell cycle were determined using the methyl thiazolyl tetrazolium ***,collagen content in HSC supernatant was evaluated by an enzyme-linked immunosorbent ***:The results showed that HMGB1 was upregulated during liver fibrosis and that its expression was closely correlated with the deposition of *** molecules were successfully transfected into HSCs and induced inhibition of HMGB1 expression in a time-dependent ***,HMGB1 siRNA treatment inhibited synthesis of α-SMA and collagen types Ⅰ and Ⅲ in transfected ***:This study suggests a significant functional role for HMGB1 in the development of liver *** also demonstrates that downregulation of HMGB1 expression might be a potential strategy to treat liver fibrosis.

关键词： Hepatic fibrosis High-mobility group box 1 Hepatic stellate cells RNA interference

Inhibition of FOXO3a/BIM signaling pathway contributes to the protective effect of salvianolic acid A against cerebral ischemia/reperfusion injury

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Acta Pharmaceutica Sinica B 2019年第3期9卷 505-515页

作者： Junke Song wen Zhang Jinhua Wang Haiguang Yang Qimeng Zhou Haigang Wang Li Li Guanhua Du State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing100050China Beijing Key Laboratory of Drug Target Identification and Drug Screening Institute of Materia MedicaChinese Academy of MedicalSciences and Peking Union Medical CollegeBeijing100050China

Salvianolic acid A(SalA) is an effective compound extracted from traditional Chinese medicine Salvia miltiorrhiza Bunge. The Forkhead box O3a(FOXO3a) signaling pathway plays crucial roles in the modulation of ischemia-induced cell apoptosis. However, no information about the regulatory effect of SalA on FoxO3a is available. To explore the anti-cerebral ischemia effect and clarify the therapeutic mechanism of SalA, SH-sy5Y cells and Sprague–Dawley rats were applied, which were exposed to oxygen glucose deprivation/reoxygenation(OGD/R) and middle cerebral artery occlusion/reperfusion(MCAO/R) injuries, respectively. The involved pathway was identified using the specific inhibitor LY294002. Results showed that SalA concentration-dependently inhibited OGD/R injury triggered cell viability loss. SalA reduced cerebral infarction, lowered brain edema, improved neurological function, and inhibited neuron apoptosis in MCAO/R rats, which were attenuated by the treatment of phosphatidylinositol-4,5-bisphosphate 3-kinase(PI3K) specific inhibitor LY294002. SalA time-and concentration-dependently upregulated the phosphorylation levels of protein kinase B(AKT) and its downstream protein FOXO3a. Moreover, the nuclear translocation of FOXO3a was inhibited by SalA both in vivo and in vitro, which was also reversed by LY294002. The above results indicated that SalA fought against ischemia/reperfusion damage at least partially via the AKT/FOXO3a/BIM pathway.

关键词： Salvianolic acid A Ischemia reperfusion FOXO3a BIM Neuroprotection

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竹材微炭化干燥工艺中液体产物特性分析

生物质化学工程 2024年第4期58卷 1-7页

作者：文世涛徐茹婷孙康陆铜华卢辛成中国林业科学研究院林产化学工业研究所江苏省生物质能源与材料重点实验室国家林业和草原局林产化学工程重点实验室林木生物质低碳高效利用国家工程研究中心江苏省林业资源高效加工利用协同创新中心江苏南京210042 千年舟新材料科技集团股份有限公司浙江杭州310000

在固定床反应器上采用微炭化工艺干燥处理竹材,并对干燥尾气进行冷凝回收,探讨微炭化干燥工艺对竹材干燥冷凝液体产物特性的影响。研究结果表明:竹材于210℃微炭化干燥处理得到冷凝液体主要含有酸、醛、酯、酮和酚类物质。微炭化工艺对... 详细信息

在固定床反应器上采用微炭化工艺干燥处理竹材,并对干燥尾气进行冷凝回收,探讨微炭化干燥工艺对竹材干燥冷凝液体产物特性的影响。研究结果表明:竹材于210℃微炭化干燥处理得到冷凝液体主要含有酸、醛、酯、酮和酚类物质。微炭化工艺对竹材干燥液体产物特性有显著影响,210℃时醛类物质质量分数达22.14%,250℃时醇、酚类物质质量分数分别为25.13%、28.33%;升温速率造成酸、醛类物质先增加后减少,10℃/min时最大,分别为67.89%、22.14%,酮类物质变化趋势则相反,20℃/min时最大,为21.35%;随氮气流量增大,酸类物质增加,由51.84%增至81.71%,醛类、酮类物质减少,分别由26.07%、10.95%降至8.36%、2.58%。竹材微炭化干燥液体产物成分与木、竹醋液相似,具有用作植物生长促进剂、土壤改良剂等潜力。

关键词：竹材微炭化干燥液体产物特性