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Journal of Analysis and Testing 2023年第2期7卷 128-135页

作者： Ni Zeng Xinyi Wang Yiyang Dong Yan Yang Yingai Yin Lianhui Zhao Xu Wang College of Life Science and Technology Beijing University of Chemical TechnologyBeijing 100029China

okadaic acid(OA),a small molecule substance derived from shellfish,is one of the most widely distributed marine toxins with acute symptoms of vomiting and diarrhea after accidental ingestion.For this,there is an urgently need for sensitive and reliable methods to detect OA in real shellfish samples.In this study,a simple aptasensor based on screen-printed carbon electrode(SPCE)with modification of chitosan(CS)and gold nanoparticles(Au NPs)was designed for electrochemical determination of OA,and the electrode surface was modified with Au NPs by potential-sweeping electrodeposition,which greatly improved the electrochemical response.The entire detection and characterization process were carried out by cyclic voltammetry(CV)with a linear correlation in the range of 0.01-100 ng/m L and a limit of detection(LOD)of 6.7 pg/m L.Furthermore,recovery rates of 92.3-116%were obtained demonstrating excellent accuracy through the recovery trial of mussel and scallop samples.

关键词： okadaic acid Aptasensor Screen-printed carbon electrode Chitosan Gold nanoparticles Cyclic voltammetry

Development of a Label-Free Colorimetric Aptasensor with Rationally Utilized Aptamer for Rapid Detection of okadaic acid

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Journal of Ocean University of China 2022年第2期21卷 400-408页

作者： YAN Xiaochen QI Xiaoyan ZHAO Yinglin LI Ling MA Rui WANG Lele WANG Sai MAO Xiangzhao College of Food Science and Engineering Ocean University of ChinaQingdao 266003China Laboratory for Marine Drugs and Bioproducts of Qingdao National Laboratory for Marine Science and Technology Qingdao 266237China

okadaic acid(OA)is a typical marine toxin with strong toxicity causing diarrheic shellfish poisoning(DSP).Aptamers show great advantages in toxin detection and attract increasing attentions in the field of food analysis.In this study,a label-free col-orimetric aptasensor was constructed for visual and rapid detection of OA in shellfish.To exploit the binding capability of the anti-OA aptamer,the inherent molecular recognition mechanism of aptamer and OA was studied,based on molecular docking,fluorescent assay,and biolayer interferometry.Consistent results showed that the stem-loop near the 3’terminal of the aptamer exhibit dominate binding capacity.Based on the revealed recognition information,the aptamer was thus rationally utilized and combined with AuNPs and cationic polymer polydiallyl dimethyl ammonium chloride(PDDA)for the development of the label-free colorimetric aptasensor,in which the 3’terminal was thoroughly exposed to OA.The aptasensor provided robust performance with a linear detection range of 100-1200 nmol L-1,a limit of detection of 41.30 nmol L-1,recovery rates of 91.6%-106.2%,as well as a high selectivity towards OA in shellfish samples.The whole detection process can be completed within 1 h.To our best knowledge,this is the first time that the anti-OA aptamer was thoroughly studied,and a label-free colorimetric aptasensor was rationally designed in this way.This study not only provides a rapid detection method for highly sensitive and specific detection of OA,but also serves as a reference for the design of efficient aptasensors in the future.

关键词： aptamer okadaic acid colorimetric aptasensor molecular docking fluorescent assay biolayer interferometry

okadaic acid: a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer's disease

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Neural Regeneration Research 2015年第3期10卷 365-367页

作者： Pradip Kumar Kamat Chandishwar Nath Division of Physiology and Biophysics University of LouisvilleSchool of Medicine Division of Pharmacology Central Drug Research Institute(CDRI)

okadaic acid： okadaic acid （OKA）, a polyether （C38 fatty acid） toxin, is a potent and selective inhibitor of protein phosphatase, PP1 and protein phosphatase 2A （PP2A）. It is mainly extracted from a black sponge Hallichondria okadaii and has been suggested to play a potent probe for studying the various molecular, cellular, biochemical and mechanism of neurotoxicity. It is known as a selective and potent in- hibitor of serine/threonine phosphatases 1 and 2A induces hyperphosphorylation of tau in vitro and in vivo. It has been reported that Alzheimer＇s disease （AD） is a complex multi- factorial neurodegenerative disorder and hyperphosphor- ylated tau protein is a major pathological hallmark of AD. The reduced activity of phosphatases like, PP2A has been implicated in the brain of AD patients. OKA also induced inhibition of protein phosphatases cause neurofibrillary tangles （NFTs） like pathological changes and tau hyperphos- phorylation seen in AD pathology. Our and others reports inferred that OKA induces neurodegeneration along with tau hyperphosphorylation, GSK3β activation, oxidative stress, neuroinflammation and neurotoxicity which are char- acteristic of AD pathology （Figure 1）.

关键词： a tool to study regulatory mechanisms for neurodegeneration and regeneration in Alzheimer’s disease okadaic acid AD

Melatonin ameliorated okadaic-acid induced Alzheimer-like lesions

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Acta Pharmacologica Sinica 2004年第3期25卷 22-26页

作者： Yi-peng WANG,Xian-tao LI,Shi-jie LIU,Xin-wen ZHOU,Xiao-chuan WANG,Jian-zhi WANG2 TongjiMedical College,Huazhong University of Science and Technology,Wuhan 430030,China Tongji Medical College Huazhong University of Science and Technology Wuhan 430030

AIM: To explore the protective effects of melatonin (Mel) on the abnormal phosphorylation of neuronal cytoskeletal proteins. METHODS: We generated a neuroblastoma (SH-SY5Y) cell system in which cytoskeletal proteins are abnormally phosphorylated resulting in microtubule disruption due to the marked inhibition of protein phosphatase activities by okadaic acid (OA). RESULTS: OA-induced declines in cell viability and mitochondrial metabolic activity were remarkably prevented by Mel. In addition, the hyperphosphorylation/accumulation of neurofilament- (NF-) H/M subunits and the disruption of microtubules, induced by OA, were significantly inhibited by Mel. CONCLUSION: Our results suggest multiple protective functions of Mel against a series of pathological lesions known to culminate in AD, including abnormal phosphorylation of cytoskeletal proteins, microtubule disassembly and mitochondrion-initiated cell toxicity.

关键词： Alzheimer disease protein phosphatase okadaic acid neurofilament proteins melatonin

Exogenous brain-derived neurotrophic factor attenuates cognitive impairment induced by okadaic acid in a rat model of Alzheimer's disease

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Neural Regeneration Research 2018年第12期13卷 2173-2181页

作者： Ai-Hua Xu Yang Yang Yong-Xin Sun Chao-Dong Zhang Department of Rehabilitation Medicine the First Affiliated Hospital of China Medical University Department of Neurology the First Affiliated Hospital of China Medical University

Decreased expression of brain-derived neurotrophic factor（BDNF） plays an important role in the pathogenesis of Alzheimer＇s disease, and a typical pathological change in Alzheimer＇s disease is neurofibrillary tangles caused by hyperphosphorylation of tau. An in vivo model of Alzheimer＇s disease was developed by injecting okadaic acid（2 μL） and exogenous BDNF（2 μL） into the hippocampi of adult male Wister rats. Spatial learning and memory abilities were assessed using the Morris water maze. The expression levels of protein phosphatase 2 A（PP2 A）, PP2 Ac-Yp307, p-tau（Thr231）, and p-tau（Ser396/404） were detected by western blot assay. The expression levels of BDNF, TrkB, and synaptophysin mRNA were measured by quantitative real-time polymerase chain reaction. Our results indicated that BDNF expression was suppressed in the hippocampus of OA-treated rats, which resulted in learning and memory deficits. Intra-hippocampal injection of BDNF attenuated this OA-induced cognitive impairment. Finally, our findings indicated an involvement of the PI3 K/GSK-3β/AKT pathway in the mechanism of BDNF in regulating cognitive function. These results indicate that BDNF has beneficial effect on Alzheimer＇s disease, and highlight the potential of BDNF as a drug target for treatment of Alzheimer＇s disease.

关键词： nerve regeneration Alzheimer＇s disease exogenous brain-derived neurotrophic factor Tau protein okadaic acid phosphorylation PP2A- Y307 glycogen synthase kinase-3~ TrkB cognitive function brain protection neural regeneration

Taxonomy and toxin profi le of harmful benthic Prorocentrum(Dinophyceae)species from the Xisha Islands,South China Sea

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Journal of Oceanology and Limnology 2022年第3期40卷 1171-1190页

作者： Jian ZOU Qun LI Hui LIU Ying LIU Lifen HUANG Haiyan WU Jiangbing QIU Hua ZHANG Songhui LÜ Research Center of Harmful Algae and Marine Biology College of Life Science and TechnologyJinan UniversityGuangzhou 510362China State Environmental Protection Key Laboratory of Drinking Water Source Management and Technology Shenzhen Academy of Environmental ScienceShenzhen 510008China Yellow Sea Fisheries Research Institute Qingdao 266071China College of Environmental Science and Engineering Ocean University of ChinaQingdao 266100China Shenzhen Academy of Environmental Science Shenzhen 510008China Southern Marine Science and Engineering Guangdong Laboratory Zhuhai 519000China

Some benthic Prorocentrum can produce okadaic acid(OA)and dinophysistoxins(DTXs)that cause diarrheic shellfish poisoning(DSP)in humans.The diversity and toxin profi les(OA and DTXs)of benthic Prorocentrum were investigated in the Xisha Islands,South China Sea.The benthic Prorocentrum was identified by both morphological features and molecular phylogenies.Morphologies were examined by light,fluorescence,and scanning electron microscopy,and phylogenetic analyses were based on partial large subunit(LSU)rDNA and ITS1-5.8S-ITS2(ITS)region.Seven Prorocentrum species including P.borbonicum,P.caipirignum,P.concavum,P.elegans,P.cf.emarginatum,P.lima complex,and P.rhathymum were identified in Xisha Islands.Among them,P.borbonicum and P.elegans were recorded in Chinese waters for the first time.OA and DTXs contents of seven benthic Prorocentrum species were evaluated based on liquid chromatography-tandem mass spectrometry(LC-MS/MS).All Xisha Islands strains of P.lima complex produced OA at contents ranging from 1663 to 3816 fg/cell.P.caipirignum also generated OA at 407 fg/cell,but other five species had no detectable toxins.Besides,interestingly,two strains of P.lima complex produced DTX-1 only(74 and 183 fg/cell)and another two strains generated an isomer of OA and DTX-2.Our findings provided insight into the biodiversity of benthic Prorocentrum in the Xisha Islands and pointed out the potential risk of DSP in this area.

关键词： Prorocentrum diversity dinofl agellate okadaic acid dinophysistoxins Xisha Islands

Effects of humanin on okadaic acid-induced tau hyperphosphorylation and neurotoxicity in neurons

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Ginsenoside Rgl Attenuates okadaic acid Induced Spatial Memory Impairment by the GSK 3β/Tau signaling pathway and the Aβ formation prevention in Rats

中国生理学会第23届全国会员代表大会暨生理学学术大会

作者： Jin-Feng ZHAO,Dan WANG,Ling-Min LI,Ce ZHANG~* Department of Physiology,Shanxi Medical University,Taiyuan 030001,China

Alzheimer’s disease(AD) is the most common human neurodegenerative disorder characterized by the progressive deterioration of cognition and memory in association with the presence of senile plaques(SP),neurofibrillary tangles(NFT),and massive loss of neurons.The NFT contain paired helical filaments(PHF),which are mostly composed of hyperphosphorylated tau.Tau is a microtubule-associated protein enriched in the axonal compartment and an imbalance of protein kinases and protein phosphatases is essential for tau abnormal hyperphosphorylation.okadaic acid(OA) is an extractive of marine life which can inhibit PP2A,one of major types of protein phosphatases,cause tau hyperphosphorylation and then result in neurotoxicity.A novel peptide termed humanin(HN) was recently reported to rescue neurons in vitro from the toxicity induced by amyloid-β(Aβ) peptides and familial AD(FAD)-linked mutant genes.Previous studies in our lab have shown that HN can attenuate exitotoxicity induced by NMDA,and inhibit neuronal insults induced by hypoxia in cortical neuron.All these results strongly suggested that HN might have a broader spectrum of protection effect.Therefore,this experiment was designed to investigate whether HN could inhibit OA-induced tau hyperphosphorylation and neurotoxicity.Results: First part is to determine OA-induced phosphorylation level of tau protein and protection of HN detected by Western -blot assays.Results showed that lower concentration of OA(5 nmol/L) has no effects,howerever,the phosphorylation level of tau protein was significantly increased when neurons were treated with OA(10 nmol/L,20 nmol/L,P0.05),while the higher concentration of HN(10μmol/L,20μmol/L) significantly inhibited OA-induced hyperphosphorylation of tau(P<0.05).It was also shown

关键词： tau protein okadaic acid hyperphosphorylation neurotoxicity,humanin

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Ginsenoside Rgl Attenuates Okadaic Acid Induced Spatial Memo...

Green tea polyphenol ameliorates spatial learning and memory impairment and tau protein hyperphosphorylation of hippocampal neurons induced by okadaic acid in rats

第二届中国药理学会补益药药理专业委员会学术研讨会

作者： Xiu-Yun Song,Jin-Feng Hu,Shi-Feng Chu,Yu-He Yuan,Jun-tian Zhang, Nai-Hong Chen~* State Key Laboratory of Bioactive Substance and Function of Natural Medicines,Institute of Mate ria Medica,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100050

There has been no extensive characterization of the effects of Ginsenoside Rg1,a pharmacological active component purified from the nature product ginseng,in an Alzheimer’s disease rats model. Objective:The present study aimed to investigate the possible neuroprotective effects of ginsenoside Rgl against okadaic acid(OKA) -induced memory impairment and the related mechanism in rat. Methods:okadaic acid,a protein phosphatase inhibitor,was used for mimic Alzheimer’s disease.After being pretreated with Rgl(5,10,20mg/kg/day,i.g) and anti-dementic drugs donepezil(1 mg/kg/day,i.g) for a week,the rats were unilaterally intracerebroventricular(ICV) microinjected with OKA(200ng),and then were continuously administrated with Rg1 and donepezil for an additional week.Next the rats were trained on a spatial memory task in Morris Water Maze(MWM) for 9 days, in which Rgl and donepezil were administrated continuously.After the behavioral test. the rats were killed for immunohistochemistry,western blotting and TUNEL staining. Results:OKA caused memory impairment in rats in MWM test remarkably with latency time prolonged and the number of times decreased passing across target area. And there were many TUNEL positive apoptotic cells observed in OKA group.Also OKA treated rats showed memory impairment including hyperphosphorylation of tau protein,the decreasing of phosphorylation glycogen synthase kinase-3β(p-GSK3β) and the formation ofβ/A4-amyloid containing plaque-like structures with immunohistochemistry and western blotting in brain regions hippocampus.Treatment with Rgl and donepezil protected ICV OKA induced memory impairment and changes in level of latency time and number of passing across target area in behavioral test,expression of p-tau and p-GSK3β,andβ/A4-amyloid accumulation, especially in 20mg/kg ginsenoside Rgl group. Conclusions:The result of the present work implied that ginsenoside Rgl protected SD rats against OA-induced toxicity.The possible neuroprotective mechanism may be that ginsenoside Rgl decreases OA-induce

关键词： Ginsenoside Rg1 okadaic acid Memory Impairment Morris Water Maze GSK 3β/Tau signaling pathway Aβformation

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Green tea polyphenol ameliorates spatial learning and memory...

Cellular and molecular mechanisms underlying the action of ginsenoside Rg1 against Alzheimer’s disease

中国生理学会第23届全国会员代表大会暨生理学学术大会

作者： Hong-Yu LI~1,Xiu-Kui WU~1,Mei-Jun SHI~1,Jun ZHANG~1,Liu JING~1,De-Zheng GONG~1,Liang ZHU~1,Li-Li GUAN~1,Qiong WU~1,Bo YUAN~1,Guo-Zhu HAN~2,Yuan ZOU~(1,*) 1 Department of Physiology 2 Faculty of Pharmacology,Dalian Medical University,Dalian 116044,China

＜正＞Objective:Green tea polyphenols（GTPs） are now being considered as possible protective agents in neurodegenerative diseases such as Alzheimer’s disease（AD）.Previous studies suggested that GTPs could inhibit amyloid fibril formation and protect neurons from toxicity induced byβ-amyloid in vitro.However,it is still unclear that whether GTPs decrease hyperphosphorylation of tau protein and ameliorate learning and memory impairments induced by okadaic acid（OA） in rats.The aim of this study is to explore the effects of GTPs on the hyperphosphorylation of tau protein and the learning and memory impairments in rats.Methods:SD rats were pretreated with GTPs by intragastric administration,and microinjected with OA into the right dorsal hippocampus.The ethological test was examined,and hyperphosphorylation of tau protein was examined both in vivo and in vitro.Results: With the increase of training,the escape latency of each group shortened gradually,and that of rats with GTPs shortened more obviously than control groups.The staying time in the target quadrant was significantly decreased after OA microinjection,whereas rats pretreated with GTPs stayed for longer time,and had a longer swimming distance in target quadrant compared with control group rats.Furthermore,GTPs could greatly attenuate the loss of primary hippocampal neurons and inhibit neurite degeneration induced by OA-induced toxicity,and also reduce the accumulation of PHF-13-positve immunoreactivity.Conclusions:These results suggested that GTPs could ameliorate OA-induced spatial memory impairment and diminish tau hyperphosphorylation.GTPs had protective effects against OA-induced neurotoxicity.These data indicated that green tea may be beneficial for preventing AD.

关键词： green tea polyphenols tau protein okadaic acid Alzheimer’s disease

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Neural Regeneration Research 2012年第36期7卷 2860-2866页

作者： Xi Li Ming Li Yuan Li Qiankun Quan Juan Wang Department of Geriatrics Second Affiliated HospitalCollege of MedicineXi’an Jiaotong University Department of Encephalopathy Xi’an Electric Power Central Hospital Research Center of Rehabilitation Science and Technology School of Life Science and TechnologyXi’an Jiaotong University Department of Laboratory Medicine Xijing HospitalFourth Military Medical University

Ginsenoside Rgl inhibits oxidation, aging and ce this study, we pretreated rat brain tissue sections I apoptosis, and improves cognitive function. In with ginsenoside Rgl, and established brain slice models of Alzheimer＇s disease induced by okadaic acid. The results revealed that ginsenoside Rgl pretreatment suppressed the increase in phosphorylated Tau protein expression induced by incubation with okadaic acid, and reduced brain-derived neurotrophic factor expression. These results suggest that ginsenoside Rgl upregulates brain-derived neurotrophic factor expression and inhibits Tau protein phosphorylation in brain slices from a rat model of Alzheimer＇s disease.

关键词： Alzheimer＇s disease ginsenoside Rgl okadaic acid phosphorylated Tau protein brain-derivedneurotrophic factor traditional Chinese medicine neural regeneration