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Neuroprotective Effect of Chrysophanol as a PI3K/AKT/mTOR Signaling Inhibitor in an Experimental Model of Autologous Blood-induced Intracerebral Hemorrhage

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Current Medical Science 2022年第2期42卷 249-266页

作者： Kuldeep Singh JADAUN Sidharth MEHAN Aarti SHARMA Ehraz Mehmood SIDDIQUI Sumit KUMAR NaifALSUHAYMI neuropharmacology division Department of PharmacologyISF College of PharmacyMogaPunjab142001India Department of Emergency Medical Services Faculty of Health Sciences-AlQunfudahUmm Al-Qura UniversityMekkahSaudi Arabia

Objective Intracerebral hemorrhage(ICH)refers to predominant,sporadic,and non-traumatic bleeding in the brain *** PI3K/AKT/mTOR signaling pathway is an important signal transduction pathway regulated by enzyme-linked receptors and has many biological functions in *** plays a key role in neuronal metabolism,gene expression regulation,and tissue homeostasis in the healthy and diseased *** In the present study,the role of the PI3K/AKT/mTOR pathway inhibitor chrysophanol(CPH)(10 mg/kg and 20 mg/kg,orally)in the improvement of ICH-associated neurological defects in rats was *** blood(20µL/5 min/unilateral/intracerebroventricular)mimics ICH-like defects involving cellular and molecular dysfunction and neurotransmitter *** current study also included various behavioral assessments to examine cognition,memory,and motor and neuromuscular *** protein expression levels of PI3K,AKT,and mTOR as well as myelin basic protein and apoptotic markers,such as Bax,Bcl-2,and caspase-3,were examined using ELISA ***,the levels of various neuroinflammatory cytokines and oxidative stress markers were ***,the neurological severity score,brain water content,gross brain pathology,and hematoma size were used to indicate neurological function and brain *** CPH was found to be neuroprotective by restoring neurobehavioral alterations and significantly reducing the elevated PI3K,AKT,and mTOR protein levels,and modulating the apoptotic markers such as Bax,Bcl-2,and caspase-3 in rat brain *** substantially reduced the inflammatory cytokines like interleukin(IL)-1β,IL-6,and tumor necrosis factor-α.CPH administration restored the neurotransmitters GABA,glutamate,acetylcholine,dopamine,and various oxidative stress *** Our results show that CPH may be a promising therapeutic approach for overcoming neuronal damage caused by the overexpression of the PI3K/AKT/mTOR signal

关键词： intracerebral hemorrhage autologous blood PI3K/AKT/mTOR hematoma chrysophanol apoptosis neurotransmitter neuroinflammation

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The uPA/uPAR system in astrocytic wound healing

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Neural Regeneration Research 2022年第11期17卷 2404-2406页

作者： Manuel Yepes division of neuropharmacology and Neurologic Diseases Yerkes National Primate Research CenterAtlantaGAUSA Department of Neurology Emory University School of MedicineAtlantaGAUSA Department of Neurology Veterans Affairs Medical CenterAtlantaGAUSA

The repair of injured tissue is a highly complex process that involves cell prolife ration,differentiation,and *** migration requires the dismantling of intercellular contacts in the injured zone and their subsequent reconstitution in the wounded ***-type plasminogen activator(u PA)is a serine proteinase found in multiple cell types including endothelial cells,smooth muscle cells,monocytes,and macrophages.A substantial body of experimental evidence with different cell types outside the central nervous system indicates that the binding of uPA to its receptor(uPAR)on the cell surface prompts cell migration by inducing plasmin-mediated degradation of the extracellular *** contrast,although uPA and uPAR are abundantly found in astrocytes and u PA binding to uPAR triggers astrocytic activation,it is unknown if uPA also plays a role in astrocytic *** cadherin is a member of cell adhesion proteins pivotal for the formation of cell-cell conta cts between *** specifically,while the extracellular domain of neuronal cadherin interacts with the extracellular domain of neuronal cadherin in neighboring cells,its intracellular domain binds toβ-catenin,which in turn links the complex to the actin cytos *** synthase kinase 3βis a serine-threonine kinase that prevents the cytoplasmic accumulation ofβ-catenin by inducing its phosphorylation at Ser33,Ser37,and Ser41,thus activating a sequence of events that lead to its proteasomal *** data discussed in this perspective indicate that astrocytes release u PA following a mechanical injury,and that binding of this u PA to uPAR on the cell membrane induces the detachment ofβ-catenin from the intracellular domain of neuronal cadherin by triggering its extracellular signal-regulated kinase 1/2-mediated phosphorylation at ***,this is followed by the cytoplasmic accumulation ofβ-catenin because uPA-induced extracellular signalregulated kinase 1/2 activ

关键词： astrocytes lipoprotein receptor-related protein 6 plasmin urokinase receptor urokinase-type plasminogen activator Wnt-β-catenin pathway wound healing β-catenin

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Urokinase-type plasminogen activator is a modulator of synaptic plasticity in the central nervous system:implications for neurorepair in the ischemic brain

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Neural Regeneration Research 2020年第4期15卷 620-624页

作者： Manuel Yepes division of neuropharmacology and Neurologic Diseases Yerkes National Primate Research Center Department of Neurology Emory University School of Medicine Department of Neurology Veterans Affairs Medical Center

The last two decades have witnessed a rapid decrease in mortality due to acute cerebral ischemia that paradoxically has led to a rapid increase in the number of patients that survive an acute ischemic stroke with various degrees of ***,the lack of an effective therapeutic strategy to promote neurological recovery among stroke survivors has led to a rapidly growing population of disabled ***,understanding the mechanisms of neurorepair in the ischemic brain is a priority with wide scientific,social and economic *** ischemia has a harmful effect on synaptic structure associated with the development of functional *** agreement with these observations,experimental evidence indicates that synaptic repair underlies the recovery of neurological function following an ischemic ***,it has become evident that synaptic plasticity is crucial not only during development and learning,but also for synaptic repair after an ischemic *** plasminogen activating system is assembled by a cascade of enzymes and their inhibitors initially thought to be solely involved in the generation of ***,recent work has shown that in the brain this system has an important function regulating the development of synaptic plasticity via mechanisms that not always require plasmin ***-type plasminogen activator(uPA)is a serine proteinase and one of the plasminogen activators,that upon binding to its receptor(uPAR)not only catalyzes the conversion of plasminogen into plasmin on the cell surface,but also activates cell signaling pathways that promote cell migration,proliferation and *** role of uPA is the brain is not fully ***,it has been reported while uPA and uPAR are abundantly found in the developing central nervous system,in the mature brain their expression is restricted to a limited group of ***,following an ischemic injury to the mature brain the expressio

关键词： cerebral ischemia neurorepair plasminogen plasticity stoke synapse urokinase urokinase receptor

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Adenylate cyclase activator forskolin alleviates intracerebroventricular propionic acid-induced mitochondrial dysfunction of autistic rats

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Neural Regeneration Research 2020年第6期15卷 1140-1149页

作者： Sidharth Mehan Saloni Rahi Aarti Tiwari Tarun Kapoor Kajal Rajdev Ramit Sharma Himanshi Khera Sourabh Kosey Umesh Kukkar Rajesh Dudi Department of neuropharmacology ISF College of PharmacyMogaPunjabIndia Department of Pharmacology Rajendra Institute of Technology&SciencesSirsaHaryanaIndia Pharmacology division CSIR-Indian Institute of Integrative MedicineJammuIndia

Neuronal mitochondrial dysfunction increases inflammatory mediators and leads to free radical generation and anti-oxidant enzymatic alterations,which are major neuropathological hallmarks responsible for *** dysfunction in autism is associated with decreased ATP levels due to reduced levels of cyclic adenosine *** models of autism were established by intracerebroventricular injection of propionic *** rat models had memory dysfunction,decreased muscle coordination and gait *** estimation of propionic acid-treated rats showed changes in enzyme activity in neuronal mitochondrial electron transport chain complexes and increases in pro-inflammatory cytokines,oxidative stress and lipid *** administration of 10,20 and 30 mg/kg adenylate cyclase activator forskolin for 15 days reversed these changes in a dose-dependent *** findings suggest that forskolin can alleviate neuronal mitochondrial dysfunction and improve neurological symptoms of rats with *** study was approved by the RITS/IAEC,SIRSA,HARYANA on March 3,2014(approval ***/IAEC/2014/03/03).

关键词： adenylate cyclase ATP autism forskolin mitochondrial dysfunction neuroinflammation oxidative stress propionic acid

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The plasminogen activating system in the pathogenesis of Alzheimer’s disease

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Neural Regeneration Research 2021年第10期16卷 1973-1977页

作者： Manuel Yepes Department of Neurology Emory University School of MedicineAtlantaGAUSA Department of Neurology Veterans Affairs Medical CenterAtlantaGAUSA division of neuropharmacology and Neurologic Diseases Yerkes National Primate Research CenterAtlantaGAUSA

Dementia is a clinical syndrome that affects approximately 47 million people worldwide and is characterized by progressive and irreversible decline of cognitive,behavioral and sesorimotor ***’s disease(AD)accounts for approximately 60–80%of all cases of dementia,and neuropathologically is characterized by extracellular deposits of insoluble amyloid-β(Aβ)and intracellular aggregates of hyperphosphorylated ***,although for a long time it was believed that the extracellular accumulation of Aβwas the culprit of the symptoms observed in these patients,more recent studies have shown that cognitive decline in people suffering this disease is associated with soluble Aβ-induced synaptic dysfunction instead of the formation of insoluble Aβ-containing extracellular *** observations are translationally relevant because soluble Aβ-induced synaptic dysfunction is an early event in AD that precedes neuronal death,and thus is amenable to therapeutic interventions to prevent cognitive decline before the progression to irreversible brain *** plasminogen activating(PA)system is an enzymatic cascade that triggers the degradation of fibrin by catalyzing the conversion of plasminogen into plasmin via two serine proteinases:tissue-type plasminogen activator(tPA)and urokinase-type plasminogen activator(uPA).Experimental evidence reported over the last three decades has shown that tPA and uPA play a role in the pathogenesis of ***,these studies have focused on the ability of these plasminogen activators to trigger plasmin-induced cleavage of insoluble Aβ-containing extracellular *** contrast,recent evidence indicates that activity-dependent release of uPA from the presynaptic terminal of cerebral cortical neurons protects the synapse from the deleterious effects of soluble Aβvia a mechanism that does not require plasmin generation or the cleavage of Aβ*** we discuss the role of the PA system in the pathogenesis of AD and

关键词： Alzheimer’s disease amyloid precursor protein amyloidβ neuroserpin plasmin plasminogen activating system plasminogen activator inhibitor-1 synapse tissue-type plasminogen activator urokinase-type plasminogen activator

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Urokinase-type plasminogen activator promotes synaptic repair in the ischemic brain

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Neural Regeneration Research 2018年第2期13卷 232-233页

作者： ariel diaz manuel yepes department of neurology and center for neurodegenerative disease emory university school of medicineAtlantaGAUSA division of neuropharmacology and neurologic diseases yerkes national primate research centerAtlantaGAUSA department of neurology veterans affairs medical centerAtlantaGAUSA

The central nervous system has a very high energy requirement. Accord- ingly, despite representing only 2% of the body＇s mass, the brain uses 20% of the total oxygen consumption. Importantly, because most of this energy is used to maintain synaptic activity, even a mild decrease in its supply to the brain has deleterious implications for synaptic function.

关键词： Urokinase-type plasminogen activator promotes synaptic repair in the ischemic brain AR TSP OGD LRP

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Understanding that Addiction Is a Brain Disorder Offers Help and Hope

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Health 2022年第6期14卷 684-695页

作者： Kenneth Blum Abdalla Bowirrat David Baron Rajendra D. Badgaiyan Panayotis K. Thanos Igor Elman Eric R. Braverman Mark S. Gold division of Addiction Research & Education Center for Psychiatry Medicine & Primary Care (Office of the Provost) Western University Health Sciences Pomona USA Department of Molecular Biology and Adelson School of Medicine Ariel University Ariel Israel Department of Psychiatry South Texas Veteran Health Care System Audie L. Murphy Memorial VA Hospital and Long School of Medicine University of Texas Health Science Center San Antonio USA Department of Psychiatry MT. Sinai School of Medicine New York USA Department of Psychology & Behavioral neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA) Research Institute on Addictions University at Buffalo Buffalo USA Department of Psychiatry Harvard School of Medicine Cambridge USA division of Personalized Medicine The Kenneth Blum Behavioral & Neurogenetic Institute (Division of iVitalize Inc.) Austin USA Department of Psychiatry Washington University School of Medicine St. Louis USA

We refute the controversial statement that addiction is not a brain disorder. Extensive peer-reviewed studies support the underlying neurobiological and neurogenetic basis of addiction’s “disease model”. In the 70s and 80s, a few clinical scientists suggested that it is possible to use behavioral training to teach controlled drinking. However, this controversial model failed drastically and increased labeling and stigmatization. Additionally, it was unhelpful in the search for treatment. Instead, we assert that addiction is a neuropsychiatric disorder characterized by a recurring desire to continue taking substances despite harmful physical and mental consequences. Work from our laboratory in 1995 supported the Reward Deficiency Syndrome (RDS) concept based on a common neurogenetic mechanism (hypodopaminergia) that underlies all substance and non-substance addictions. Non-substance addictions include behaviors like pathological gambling, internet addiction, and mobile phone addiction. Certain impulsive and compulsive behaviors or the acute intake of psychoactive substances result in heightened dopaminergic activity, while the opposite, hypodopaminergia, occurs following chronic abuse. Patients with Substance Use Disorder (SUD) can have a genetic predisposition compounded by stress or other epigenetic insults that can impact recovery. Relapse will occur post-short-term recovery if dopaminergic dysfunction remains untreated. Addiction, a brain disorder, requires treatment with DNA-directed pro-dopamine regulation and rehabilitation.

关键词： Reward Deficiency Syndrome Abstinence Controlled Drinking Neurogenetic Brain Disorder

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基于多尺度计算方法的活体磁共振谱自动相位矫正和代谢物定量分析(英文)

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波谱学杂志 2014年第1期31卷 32-39页

作者：张晓东胡小平 Yerkes Imaging Center and division of neuropharmacology and Neurologic Diseases Yerkes National Primate Research Center Emory University Biomedical Imaging Technique Center The Wallace H. Coulter Department of Biomedical EngineeringEmory University and Georgia Institute of Technology

活体多片磁共振谱成像(MRSI)产生大量的波谱数据,因此需要使用自动的谱数据分析方法来获得不同组织代谢产物的定量分布图.然而,活体波谱通常产生严重的谱和基线变形,使得基于曲线拟合的谱定量数据分析方法失效.该文应用多尺度分析(Multi... 详细信息

活体多片磁共振谱成像(MRSI)产生大量的波谱数据,因此需要使用自动的谱数据分析方法来获得不同组织代谢产物的定量分布图.然而,活体波谱通常产生严重的谱和基线变形,使得基于曲线拟合的谱定量数据分析方法失效.该文应用多尺度分析(Multiscale)方法自动确定兴趣代谢物在频率空间的谱峰特征(位置和线宽),然后通过叠代运算对该代谢物对应的谱峰进行独立的自动相位矫正和线型拟合.大脑波谱成像的实验结果表明,该方法可以方便、有效的获得代谢产物在大脑的分布,特别适宜于多片磁共振谱成像的代谢产物定量分析.

关键词：活体多片磁共振谱成像(MRSI) 多尺度分析方法线型拟合自动相位矫正

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The consequences of reducing expression of the 7 nicotinic receptor by RNA interference and of stimulating its activity with an 7 agonist in SH-SY5Y cells indicate that this receptor plays a neuroprotective role in connection with the pathogenesis of Alzhe

The consequences of reducing expression of the 7 nicotinic r...

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作者：齐晓岚 Agneta Nordeberg Department of Pathology and Molecular Biology Guiyang Medical University Guiyang 550004GuizhouP.R.of China Department of Neurobiology Care Medicine and Society Division of Molecular NeuropharmacologyKarolinska InstitutetS-141 86 StockholmSweden

In order to examine the neuroprotective effects of theα7 nicotinic receptor(nAChR) in relationship to the pathogenesis of Alzheimer’s disease(AD),neuroblastoma(SH-SY5Y) cells were transfected with small interference RNAs(siRNAs) that targetes specifically towardsα7 nAChR or exposed to 20 M 3- [2,4-dimethoxybenzylidene]anabaseine(DMXB),a selective agonist of this same *** levels ofα7 nAChR mRNA and protein were measured by RT-PCR and Western blotting,*** levels of theα-form of secreted amyloid precursor protein(αAPPs),total APP and the extracellular signal-regulated kinase 1/2(ERK 1/2) were also determined by Western ***-SY5Y cells transfected with siRNA or exposed to DMXB were then treated with 1μM A 25-35,following which the levels of lipid peroxidation and rate of reduction of MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide]were characterized by utilizing spectrophotometric *** to controls,SH-SY5Y cells transfected with siRNA expressed the decreases in the levels ofα7 nAChR mRNA and protein by 81%and 69%lower levels, respectively;exhibited reduced levels of theαAPPs and ERK 1/2 proteins;and demonstrated enhanced lipid peroxidation and a decreased rate of MTT *** cells exposed to DMXB,the level ofα7 nAChR protein was elevated by 23%,with no alteration in the content of the corresponding mRNA;the levels of theαAPPs and ERK 1/2 proteins were *** of the expression of theα7 nAChR gene enhanced the toxicity exerted by Aβ,whereas stimulation of this receptor attenuated this toxicity *** findings indicate thatα7 nAChR may play a significant neuroprotective role by enhancing cleavage of APP by -secretase,regulating signal transduction,improving antioxidant defenses and inhibiting the toxicity of A,which is connected with the pathogenesis of AD.

关键词： RNA interference α7 nicotinic receptor amyloid precursor protein extracellular signal-regulated kinase SH-SY5Y cells

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Hypothesizing That Pediatric Autoimmune Neuropsychiatric Associated Streptococcal (PANDAS) Causes Rapid Onset of Reward Deficiency Syndrome (RDS) Behaviors and May Require Induction of “Dopamine Homeostasis”

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Open Journal of Immunology 2022年第3期12卷 65-75页

作者： Kenneth Blum Catherine A. Dennen Eric R. Braverman Ashim Gupta David Baron Bernard William Downs Debasis Bagchi Panayotis Thanos Maureen Pollock Jag Khalsa Igor Elman Abdalla Bowirrat Rajendra D. Badgaiyan Center for Mental Health and Sports Psychiatry Western University Health Sciences Pomona USA The Kenneth Blum Behavioral & Neurogenetic Institute Austin USA Department Psychiatry Boonshoff School of Medicine Wright University Dayton USA Institute of Psychology ELTE E&#246tv&#246s Loránd University Budapest Hungary Department of Psychiatry School of Medicine University of Vermont Burlington USA division of Nutrigenomics Victory Nutrition International Inc. Bonita Springs USA Department of Molecular Biology Adelson School of Medicine Ariel University Ariel Israel Department of Family Medicine Jefferson Health Northeast Philadelphia USA Future Biologics Lawrenceville USA Department of Pharmaceutical Sciences Texas Southern University Houston USA Department of Psychology & Behavioral neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA) Research Institute on Addictions University at Buffalo Buffalo USA Department of Microbiology Immunology and Tropical Medicine School of Medicine George Washington University Washington DC USA Cambridge Health Alliance Harvard Medical School Cambridge USA Department of Psychiatry Ichan School of Medicine at Mount Sinai New York USA Department of Psychiatry South Texas Veteran Health Care System Audie L. Murphy Memorial VA Hospital Long School of Medicine University of Texas Health Science Center San Antonio USA

Pediatric autoimmune neuropsychiatric disorders associated with group A streptococcal infections (PANDAS) is a concept that is used to characterize a subset of children with neuropsychiatric symptoms, tic disorders, or obsessive-compulsive disorder (OCD), whose symptoms are exacerbated by group A streptococcal (GAS) infection. PANDAS has been known to cause a sudden onset of reward deficiency syndrome (RDS). RDS includes multiple disorders that are characterized by dopaminergic signaling dysfunction in the brain reward cascade (BRC), which may result in addiction, depression, avoidant behaviors, anxiety, tic disorders, and/or OCD. According to research by Blum et al., the dopamine receptor D2 (DRD2) gene polymorphisms are important prevalent genetic determinants of RDS. The literature demonstrates that infections like Borrelia and Lyme, as well as other infections like group A beta-hemolytic streptococcal (GABHS), can cause an autoimmune reaction and associated antibodies target dopaminergic loci in the mesolimbic region of the brain, which interferes with brain function and potentially causes RDS-like symptoms/behaviors. The treatment of PANDAS remains controversial, especially since there have been limited efficacy studies to date. We propose an innovative potential treatment for PANDAS based on previous clinical trials using a pro-dopamine regulator known as KB220 variants. Our ongoing research suggests that achieving “dopamine homeostasis” by precision-guided DNA testing and pro-dopamine modulation could result in improved therapeutic outcomes.

关键词： PANDAS CANS Reward Deficiency Syndrome Group A Beta-Hemolytic Streptococcal (GABHS) Pro-Dopamine Regulation Dopamine Homeostasis Molecular Mimicry Lyme Borrelia

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