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Design of Lipophilic Split Aptamers as Artificial Carriers for Transmembrane Transport of Adenosine triphosphate

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CCS Chemistry 2021年第11期3卷 144-153页

作者： Qiaoshu Chen Meiling Jian Hui Chen Bing Zhou Hui Shi Xiaohai Yang Kemin Wang Jianbo Liu State Key Laboratory of Chemo/Biosensing and Chemometrics College of Chemistry and Chemical EngineeringKey Laboratory for Bio-Nanotechnology and Molecular Engineering of Hunan ProvinceHunan UniversityChangsha 410082

Transmembrane transport plays an important role in many physiological functions,and mimicking this biological process in artificial systems has potential applications in biosensing,drug delivery,and bionic science.Here,a lipophilic split aptamer was developed as a novel transmembrane carrier for Adenosine triphosphate(ATP)transport.The ATP carrier comprises two split aptamer fragments and cholesterol tags,with the split aptamers acting as targetrecognition domains to enhance their specific binding capability and the cholesterol tags as hydrophobic domains to facilitate membrane penetration.Giant unilamellar vesicle experiments demonstrated that the ATP carrier-mediated transmembrane transport was concentration-and time-dependent and showed high transport selectivity.Moreover,the artificial carriers were applicable to living cells and facilitated rapid cell internalization of fluorescencelabeled ATP.Furthermore,carrier-mediated ATP transport into ATP-deficient cells enabled recovery of cellular ATP levels and improved cell viability.This study demonstrated the efficacy of an aptamer nanostructure for designing DNA-based synthetic carriers with high selectivity and flexibility.

关键词： DNA aptamer Adenosine triphosphate transmembrane transportation artificial carrier mass transportation

Autophagy occurs within an hour of Adenosine triphosphate treatment after nerve cell damage:the neuroprotective effects of Adenosine triphosphate against apoptosis

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Neural Regeneration Research 2014年第17期9卷 1599-1605页

作者： Na Lu Baoying Wang Xiaohui Deng Honggang Zhao Yong Wang Dongliang Li Department of Physiology and Neurobiology Xinxiang Medical University Department of Human Anatomy Xinxiang Medical University Department of Laboratory Animal Center Xinxiang Medical University

After hypoxia, ischemia, or inflammatory injuries to the central nervous system, the damaged cells release a large amount of Adenosine triphosphate, which may cause secondary neuronal death. Autophagy is a form of cell death that also has neuroprotective effects. Cell Counting Kit assay, monodansylcadaverine staining, flow cytometry, western blotting, and real-time PCR were used to determine the effects of exogenous Adenosine triphosphate treatment at different concentrations （2, 4, 6, 8, 10 mmol/L） over time （1, 2, 3, and 6 hours） on the apoptosis and autophagy of SH-SY5Y cells. High concentrations of extracellular Adenosine triphosphate induced autophagy and apoptosis of SH-SYSY cells. The enhanced autophagy first appeared, and peaked at 1 hour after treatment with Adenosine triphosphate. Cell apoptosis peaked at 3 hours, and persisted through 6 hours. With prolonged exposure to the Adenosine triphosphate treatment, the fraction of apoptotic cells increased. These data suggest that the SH-SY5Y neural cells initiated autophagy against apoptosis within an hour of Adenosine triphosphate treatment to protect themselves against injury.

关键词： nerve regeneration neurons Adenosine triphosphate SH-SY5Y cells autophagy apoptosis cell culture monodansylcadaverine flow cytometry cell viability Bcl-2 Bax Beclin 1 neuronal damage NSFC grant neural regeneration

Adenosine triphosphate promotes locomotor recovery after spinal cord injury by activating mammalian target of rapamycin pathway in rats

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Neural Regeneration Research 2013年第2期8卷 101-110页

作者： Zhengang Sun Lingyun Hu Yimin Wen Keming Chen Zhenjuan Sun Haiyuan Yue Chao Zhang Department of Spine Surgery First People's Hospital of Qingdao Economic & Technological Development Area Second Clinical Medical College Lanzhou University Department of Orthopedics Nanchong Central Hospital Department of Spine Surgery Lanzhou General Hospital of Lanzhou Military Region Department of Information Qingdao Eighth People's Hospital

The mammalian target of rapamycin （mTOR） pathway plays an important role in neuronal growth, proliferation and differentiation. To better understand the role of mTOR pathway involved in the induction of spinal cord injury, rat models of spinal cord injury were established by modified Allen＇s stall method and interfered for 7 days by intraperitoneal administration of mTOR activator Adenosine triphosphate and mTOR kinase inhibitor rapamycin. At 1-4 weeks after spinal cord injury induction, the Basso, Beattie and Bresnahan locomotor rating scale was used to evaluate rat locomotor function, and immunohistochemical staining and western blot analysis were used to detect the expression of nestin （neural stem cell marker）, neuronal nuclei （neuronal marker）, neuron specific enolase, neurofilament protein 200 （axonal marker）, glial fibrillary acidic protein （astrocyte marker）, Akt, mTOR and signal transduction and activator of transcription 3 （STAT3）. Results showed that Adenosine triphosphate-mediated Akt/mTOR/STAT3 pathway increased endogenous neural stem cells, induced neurogenesis and axonal growth, inhibited excessive astrogliosis and improved the locomotor function of rats with spinal cord injury.

关键词： neural regeneration spinal cord injury serine/threonine-specific protein kinase mammalian target ofrapamycin pathway signal transduction and activator of transcription 3 Adenosine triphosphate signal pathway rapamycin photographs-containing paper neuroregeneration

Effects of repetitive transcranial magnetic stimulation on Adenosine triphosphate content and microtubule associated protein-2 expression after cerebral ischemia-reperfusion injury in rat brain

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Chinese Medical Journal 2008年第14期121卷 1307-1312页

作者： FENG Hong-lin YAN Li CUI Li-ying Department of Neurology First Hospital of Harbin Medical University Harbin Heilongjiang 150001 China Department of Neurology China-Japan Friendship Hospital of Beijing Beijing 100029 China Department of Neurology Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100730 China

Background Repetitive transcranial magnetic stimulation （rTMS） research has mainly been focused on the therapeutic effect of psychiatric disorders and Parkinson＇s disease. A few studies have shown that rTMS might protect against delayed neuronal death induced by transient ischemia, enhance long-term potentiation in ischemic conditions and affect regional brain blood flow and metabolism. The aim of this study was to determine the effects of repetitive transcranial magnetic stimulation （rTMS） on Adenosine triphosphate （ATP） content and microtubule associated protein-2 （MAP-2） expression in rat brain after middle cerebral artery occlusion （MCAO）/reperfusion. Methods To study the effects of different timecourses of rTMS on ATP content and MAP-2 expression, 90 rats were randomly divided into three groups （30 rats in each group）. To study the effects of multiple rTMS parameters on ATP content and MAP-2 expression, the rats in each group were further divided into six subgroups （five rats each）. The rats were sacrificed at 1-hour, 24-hour and 48-hour intervals after reperfusion, and the brain tissues were collected for the detection of ATP and MAP-2. Results rTMS could significantly increase ATP content and MAP-2 expression in the left brain following ischemic insult （P 〈0.01） and different rTMS parameters had different effects on the ATP level and the MAP-2 expression in the left striatum. A high-frequency rTMS played an important role in MAP-2 expression and ATP preservation. Conclusions This study revealed that rTMS induced significant increase of ATP content and MAP-2 expression in the injured area of the brain, suggesting that the regulation of both ATP and MAP-2 may be involved in the biological mechanism of the effect of rTMS on neural recovery. Therefore, rTMS may become a potential adjunctive therapy for ischemic cerebrovascular disease.

关键词： transcranial magnetic stimulation repetitive cerebral ischemia-reperfusion injury Adenosine triphosphate microtubule associated protein-2

Freshness determination of royal jelly by analyzing decomposition products of Adenosine triphosphate

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Freshness determination of royal jelly by analyzing decompos...

Mitochondrial dysfunction in a rat model and the related risk of metabolic disorders

二十一世纪第二届全国蜂业科技与蜂产业发展大会

作者：吴黎明 Yue Wei Bing Du Lanzhen Chen Yong Wang Yi Li Jing Zhao XiaoFeng Xue Institute of Apiculture Research Chinese Academy of Agricultural Sciences Risk Assessment Laboratory for Bee Products Quality and Safety of Ministry of Agriculture Department of Food Science and Engineering School of Chemical EngineeringNorthwest University

Royal jelly（RJ）,widely used in food products,is highly perishable.To ensure its quality,it is necessary to identify an indicator of RJ freshness.In this study,we measured the concentrations of Adenosine triphosphate（ATP）,adenosine diphosphate（ADP）,adenosine monophosphate（AMP）,inosine monophosphate（IMP）,inosine（HxR）,hypoxanthine（Hx）,adenosine（Ao）,and adenine（Ai） in RJ stored at different temperatures and for different storage periods.An F-value,defined as ratio between the sum of Ao,Ai,HxR,and Hx and the sum of ATP,ADP,AMP,IMP,HxR,Hx,Ao,and Ai,was evaluated as an indicator of RJ freshness.When the F-value of an RJ sample was evaluated,the equivalent biochemical age could be determined based on linear equations.An F-value of 20%,with an equivalent biochemical age of 60.69 days when stored at 4℃ or 6.82 days when stored at 30℃,was the calculated RJ freshness threshold value in this study.This novel indicator could contribute to the establishment of standardized criteria for the identification of RJ freshness and provide more rigorous standards for harvesting,packaging,and storage procedures of RJ.

关键词： Royal jelly Freshness Adenosine triphosphate

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Journal of Traditional Chinese Medicine 2023年第1期43卷 95-104页

作者： LI Han HUANG Xiaomin CAI Haiyang HEROK George HE Jing SU Yixun LI Weihong YI Chenju OLIVER Brian G CHEN Hui Faculty of Basic Medical Sciences Chengdu University of Traditional Chinese MedicineChengdu 611137China Research Centre the Seventh Affiliated Hospital of Sun Yat-Sen UniversityShenzhen 518107China School of Life Sciences University of Technology SydneyNew South Wales 2059Australia

OBJECTIVE:To explore whether kidney Yang deficiency(KYD)is prone to metabolic disorders may be linked to impaired mitochondrial function in thermogenesis and metabolic tissues.METHODS:A rat model of KYD was used,which was established using Sprague Dawley rat dams with warm preference subjected to herbal treatment that can improve kidney Yang.The human relevance was confirmed by reduced serum corticosterone levels,and increased preference for warm location.RESULTS:KYD Rats were underdeveloped.adenosinetriphosphate(ATP)production was reduced in the brown fat,but increased in the muscle.However,oxidative phosphorylated complexes to generate ATP and mitochondrial biogenesis marker were reduced in both tissues.When the second insult of high-fat diet(HFD)was introduced,KYD rats gained less weight yet developed more severe lipid and glucose metabolic disorders.This may be driven by disregulated liver gluconeogenesis marker forkhead box protein O1 and lipid metabolic regulator cholesterol 7 alpha-hydroxylase.CONCLUSION:KYD rats exhibited reduced mitochondrial function in the brown fat,but were partially compensated by skeletal muscle,associated with the phenotype of warm preference and metabolic disorder,which was further exacerbated by additional HFD consumption.Future studies can focus on treatment targetting mitochondria function to reverse this phenotype.

关键词： kidney Yang deficiency DNA,mitochondrial Adenosine triphosphate thermogenesis peroxisome proliferator-activated receptor gamma coactivator 1-alpha

Mitochondrial dysfunction as a target in spinal cord injury:intimate correlation between pathological processes and therapeutic approaches

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Neural Regeneration Research 2023年第10期18卷 2161-2166页

作者： Julieta Schmidt Héctor Ramiro Quintá Universidad de Buenos Aires CABAArgentina Laboratorio de Medicina Experimental“Dr.J.Toblli” Hospital AlemánCABAArgentina Consejo Nacional de Investigaciones Científicas y Técnicas-CONICET CABAArgentina Rehabilitation Medicine Department University of MinnesotaTwin CitiesMINUSA

Traumatic spinal cord injuries interrupt the connection of all axonal projections with their neuronal targets below and above the lesion site. This interruption results in either temporary or permanent alterations in the locomotor, sensory, and autonomic functions. Damage in the spinal tissue prevents the re-growth of severed axons across the lesion and their reconnection with neuronal targets. Therefore, the absence of spontaneous repair leads to sustained impairment in voluntary control of movement below the injury. For decades, axonal regeneration and reconnection have been considered the opitome of spinal cord injury repair with the goal being the repair of the damaged long motor and sensory tracts in a complex process that involves:(1) resealing injured axons;(2) reconstructing the cytoskeletal structure inside axons;(3) re-establishing healthy growth cones;and(4) assembling axonal cargos. These biological processes require an efficient production of Adenosine triphosphate, which is affected by mitochondrial dysfunction after spinal cord injury. From a pathological standpoint, during the secondary stage of spinal cord injury, mitochondrial homeostasis is disrupted, mainly in the distal segments of severed axons. This result in a reduction of Adenosine triphosphate levels and subsequent inactivation of Adenosine triphosphate-dependent ion pumps required for the regulation of ion concentrations and reuptake of neurotransmitters, such as glutamate. The consequences are calcium overload, reactive oxygen species formation, and excitotoxicity. These events are intimately related to the activation of necrotic and apoptotic cell death programs, and further exacerbate the secondary stage of the injury, being a hallmark of spinal cord injury. This is why restoring mitochondrial function during the early stage of secondary injury could represent a potentially effective therapeutic intervention to overcome the motor and sensory failure produced by spinal cord injury. This review discusses the most recent evidence linkin

关键词： Adenosine triphosphate axonal regeneration creatine mitochondria dysfunction mitochondria spinal cord injury

Mitochondria targeting drugs for neurodegenerative diseases——Design, mechanism and application

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Acta Pharmaceutica Sinica B 2022年第6期12卷 2778-2789页

作者： Jiajia Xu Wei Du Yunhe Zhao Kahleong Lim Li Lu Chengwu Zhang Lin Li Key Laboratory of Flexible Electronics(KLOFE)&Institute of Advanced Materials(IAM) Jiangsu National Synergetic Innovation Center for Advanced Materials(SICAM)Nanjing Tech University(NanjingTech)Nanjing 211816China Department of Anatomy Shanxi Medical UniversityTaiyuan 030001China Lee Kang Chian School of Medicine Nanyang Technological UniversitySingapore 308232Singapore School of Basic Medical Sciences Shanxi Medical UniversityTaiyuan 030001China The Institute of Flexible Electronics(IFE Future Technologies)Xiamen UniversityXiamen 361005China

Neurodegenerative diseases(NDDs) such as Alzheimer’s disease(AD) and Parkinson ’s disease(PD) are a heterogeneous group of disorders characterized by progressive degeneration of neurons.NDDs threaten the lives of millions of people worldwide and regretfully remain incurable.It is well accepted that dysfunction of mitochondria underlies the pathogenesis of NDDs.Dysfunction of mitochondria results in energy depletion,oxidative stress,calcium overloading,caspases activation,which dominates the neuronal death of NDDs.Therefore,mitochondria are the preferred target for intervention of NDDs.So far various mitochondria-targeting drugs have been developed and delightfully some of them demonstrate promising outcome,though there are still some obstacles such as targeting specificity,delivery capacity hindering the drugs development.In present review,we will elaborately address 1) the strategy to design mitochondria targeting drugs,2) the rescue mechanism of respective mitochondria targeting drugs,3) how to evaluate the therapeutic effect.Hopefully this review will provide comprehensive knowledge for understanding how to develop more effective drugs for the treatment of NDDs.

关键词： Neurodegenerative diseases Mitochondria Targeting drug Apoptosis Reactive oxygen species Adenosine triphosphate Mitochondrial membrane potential Evaluation

Blockage of ATPase-mediated energy supply inducing metabolic disturbances in algal cells under silver nanoparticles stress

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Journal of Environmental Sciences 2023年第9期131卷 141-150页

作者： Ruohua Qu Mi Chen Jingfu Liu Qiting Xie Na Liu Fei Ge Department of Environment College of Environment and ResourcesXiangtan UniversityXiangtan 411105China State Key Laboratory of Environmental Chemistry and Ecotoxicology Research Center for Eco-Environmental SciencesChinese Academy of SciencesBeijing 100085China

Adenosine triphosphate(ATP)generation of aquatic organisms is often subject to nanoparticles(NPs)stress,involving extensive reprogramming of gene expression and changes in enzyme activity accompanied by metabolic disturbances.However,little is known about the mechanism of energy supply by ATP to regulate the metabolism of aquatic organisms under NPs stress.Here,we selected extensively existing silver nanoparticles(AgNPs)to investigate their implications on ATP generation and relevant metabolic pathways in alga(Chlorella vulgaris).Results showed that ATP content significantly decreased by 94.2%of the control(without AgNPs)in the algal cells at 0.20 mg/L AgNPs,which was mainly attributed to the reduction of chloroplast ATPase activity(81.4%)and the downregulation of ATPase-coding genes atpB and atpH(74.5%-82.8%)in chloroplast.Molecular dynamics simulations demonstrated that AgNPs competed with the binding sites of substrates adenosine diphosphate and inorganic phosphate by forming a stable complex with ATPase subunit beta,potentially resulting in the reduced binding efficiency of substrates.Furthermore,metabolomics analysis proved that the ATP content positively correlated with the content of most differential metabolites such as D-talose,myo-inositol,and L-allothreonine.AgNPs remarkably inhibited ATPinvolving metabolic pathways,including inositol phosphate metabolism,phosphatidylinositol signaling system,glycerophospholipid metabolism,aminoacyl-tRNA biosynthesis,and glutathione metabolism.These results could provide a deep understanding of energy supply in regulating metabolic disturbances under NPs stress.

关键词： Adenosine triphosphate Metabolomics Molecular dynamics simulations Nanoparticles Algae