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Aged rat heart: Modulation of age-related respiratory defects decreases ischemic-reflow injury

Health 2013年第1期5卷 1-7页

作者： Edward J. Lesnefsky Charles L. Hoppel Center for Mitochondrial Diseases Departments of Medicine and Pharmacology Case Western Reserve University Cleveland USA departments of medicine Biochemistry and Physiology Virginia Commonwealth University and McGuire Veterans Affairs Medical Center Richmond USA

Myocardial injury increases in the elderly heart during ischemia and reperfusion. Mitochondria, the key targets and sources of injury during ischemia and reperfusion, sustain ischemic damage to the electron transport chain that is superimposed upon age-related defects. In the adult heart, interventions to activate endogenous cytoprotective signaling systems meet in mitochondria to decrease cardiac injury. Unfortunately, these systems are largely ineffective in the aged heart. Thus, new treatment concepts are needed to reduce injury in the aged heart. Our group chose a strategy to directly treat the effector of cardiac injury in the aged heart, the mitochondria. We further utilized a novel approach to ask if the reversal of aging defects in cardiac mitochondria before ischemia could decrease ischemia-reperfusion injury in the heart. Three hours following treatment with the small molecule, nutriceutical acetylcarnitine (AcCN), oxidative phosphorylation as well as age-induced defects in electron transport chain complexes III and IV was corrected in the heart. When such hearts were then exposed to ischemia and reperfusion, cardiac injury was markedly reduced. Contraction during reperfusion improved and recovery became similar to that in adult hearts. Cardiac cell death was substantially reduced. Thus, age-related defects in electron transport are a key mechanism of the increased myocardial injury in the elderly heart during ischemia and reperfusion. Modulation of aging-induced defects in mitochondrial metabolism reduces cardiac injury from ischemia and reperfusion, and is a novel strategy to protect myocardium in the elderly patient at risk for an acute myocardial infarction.

关键词： Mitochondria Cytochrome Oxidase Complex III Myocardial Infarction Aging

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S2A-5 Targeting PDE4 for Alzheimer’s Disease and Alcoholism:An implication in Alcohol-Related Dementia?

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神经药理学报 2018年第4期8卷 39-41页

作者： WANG Hao ZHANG Fang-fang FU Hua-rong ZHOU Yan-meng LIU Xin HOU Xue-qin HU Wei Rolf Hansen XU Ying James O’Donnell 张汉霆 Institute of pharmacology the First Medical University of ShandongTai’an271016China departments of behavioral medicine&psychiatry Physiology&Pharmacologyand Neurosciencethe Rockefeller Neurosciences InstituteWest Virginia University Health Sciences CenterMorgantownWV 26506USA Department of Pharmaceutical Sciences School of Pharmacy&Pharmaceutical SciencesState University of New York at BuffaloBuffaloNY 14214USA

Background:Phosphodiesterase 4(PDE4),one of the 11 PDE enzyme families that hydrolyze cyclic nucleotides,is critical for controlling intracellular cyclic AMP(cAMP)concentrations and plays an important role in regulating alcohol consumption and mediating memory in dementia such as Alzheimer’s disease(AD).Chronic alcohol consumption can cause alcohol-related dementia and 50%~75%of detoxified alcoholics have memory or cognition ***,the role of PDE4 and its mechanism remain to be characterized and ***:Using the water-maze,passive avoidance,or novel object recognition test,we examined the effects of rolipram,a prototypical PDE4 inhibitor,and roflumilast,a potent PDE4 inhibitor which has been approved for treatment of chronic obstructive pulmonary disease(COPD)in humans,on memory loss in APP/PS1 double transgenic mice,a widely used model for *** addition,we tested the effects of the PDE4 inhibitors,via ip,intra-gastric,or intrastriatum infusion,on ethanol intake and preference using the mouse two-bottle choice *** deficient in PDE4A,PDE4B,or PDE4D(4AKO,4BKO,and 4DKO,respectively)and their wild type(WT)controls were tested for ethanol consumption and memory;the latter was measured in the absence or presence of beta-amyloid peptide 1-42(Abeta42)infused into the dorsal ***:Similar to rolipram,roflumilast reversed memory deficits in APP/PS1 mice in all the memory tests and reduced ethanol intake and preference in C57BL/6 mice in two-bottle *** with the results in the memory tests,roflumilast reduced the loss of neurons and neurocyte apoptosis in AD mice,as shown using HE and Nissl *** also reversed the decreased ratio of Bcl-2/BAX in the cerebral cortex and hippocampus of AD *** addition,roflumilast reversed the decreased levels of cAMP and expression of phosphorylated cAMP response element-binding protein(CREB)and brain derived neurotrophic factor(BDNF)in AD *** to the WT controls,4

关键词： Phosphodiesterase-4(PDE4) Alzheimer’s disease(AD) alcoholism cAMP signaling memory trangenic mice

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NP-3 Effects of Osthole Microemulsion by Nasal Administration on the Cholinergic Pathway in AD Mice

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神经药理学报 2018年第4期8卷 101-102页

作者： HOU Xue-qin RONG Cui-ping HAO Ji-fu ZHANG Han-ting Institute of pharmacology Taishan Medical UniversityShandong271016China Guangxi Key Laboratory of Brain and Cognitive Neuroscience Guilin Medical UniversityGuilinChina Department of Pharmacy Taishan Medical UniversityShandong271016China departments of behavioral medicine&psychiatry Physiology&Pharmacologyand Neurosciencethe Rockefeller Neurosciences InstituteWest Virginia University Health Sciences CenterMorgantownWV 26506USA

Objectives:Fructus Cnidii is the dry ripe fruit of Cnidium monnieri(L.)Cuss.,which belongs to the umbelliferous *** has long been used in clinic practice and has been found to have pharmacological activity in the central nervous *** is the main active component of Fructus ***,it shows low bioavailability,fast distribution and elimination,and low concentration in the brain when given *** this study,we aimed to develop a new dosage form to increase the osthole concentration in the brain and enhance its pharmacological effects in the central nervous system through reducing the dosage while improving the stability and ***,microemulsion containing osthole was prepared and the effects of osthole microemulsion were examined in the mouse model of Alzheimer’s disease(AD).Methods:On the basis of pseudo-ternary phase diagram,microemulsion was prepared by using polyoxyethlated Cremophor RH40 as emulsifiers,propylene glycol as assistant emulsifiers and ethyl acetate as the oil *** particle size and distribution of osthole microemulsion were detected by laser particle size analyzer and transmission election *** content of osthole was determined by UV *** effects of osthole microemulsion by nasal administration on the learning and memory abilities in scopolamine-treated mice were assessed by Morris water maze and novel object recognition *** superoxide dismutase(SOD)activity,glutathione(GSH)levels and malondialdehyde(MDA)contents in the serum were examined to evaluate the oxidant *** acetyltransferase(ChAT)and acetylcholinesterase(AChE)expression in the olfactory-basal forebrain pathway were detected by immunohistochemical *** also investigated the acetylcholine(ACh)levels and the histological morphology in the ***:The average particle size of 1μg·μL-1 osthole microemulsion was less than 15 *** was characterized as spheres under the transmission electron micros

关键词： Osthole nanoemulsions Pseudo-ternary phase diagram Nasal administration Cholinergic nerve circuits

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An international guideline with six personalised titration schedules for preventing myocarditis and pneumonia associated with clozapine

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General psychiatry 2022年第3期35卷 157-162页

作者： Jose de Leon Can-Jun Ruan Georgios Schoretsanitis Christopher Rohde Elif Anıl Yağcıoğlu Trino Baptista Oleg O Kirilochev Carlos De las Cuevas Christoph U Correll Mental Health Research Center Eastern State HospitalLexingtonKentuckyUSA 2 Biomedical Research Centre in Mental Health Net(CIBERSAM)Hospital Santiago ApóstolVitoria-GasteizSpain 3 Laboratory of Clinical PsychopharmacologyBeijing An Ding HospitalBeijingChina 4 The National Clinical Research Centre for Mental Disorders&Beijing Key Lab of Mental DisordersBeijing An Ding HospitalBeijingChina 5 PsychiatryUniversity of ZürichZurichSwitzerland 6 Psychiatry ResearchZucker Hillside HospitalGlen OaksNew YorkUSA 7 Affective DisordersAarhus University HospitalAarhusDenmark 8 Clinical MedicineAarhus UniversitetAarhusDenmark 9 PsychiatryHacettepe UniversitesiAnkaraTurkey 10PhysiologyLos Andes University Medical SchoolMeridaBolivarian Republic of Venezuela 11Clinical PharmacologyAstrakhan State Medical UniversityAstrakhanAstrahanskaâRussian Federation 12Department of Internal MedicineDermatology and Psychiatry and Instituto Universitario de Neurociencia(IUNE)Universidad de La LagunaLa LagunaSpain 13Child and Adolescent PsychiatryCharitéUniversitätsmedizin BerlinBerlinGermany

White blood cell(WBC)monitoring has reduced clozapinetreated patient deaths associated with agranulocytosis to a ***,clozapine protocols and package inserts worldwide provide no instructions for preventing myocarditis or pneumonia during clozapine *** worldwide are largely unaware of ***,as they worry about agranulocytosis,their clozapine-treated patients are at risk of dying from pneumonia or ***,an international guideline with 104 authors from 50 countries/regions was recently published to provide personalised clozapine titration schedules for adult *** forum article reviews pneumonia and myocarditis occurring during clozapine titration,as well as the three most innovative aspects of this new guideline:(1)personalised titration,(2)C reactive protein(CRP)measures,and(3)dose predictions based on blood *** metabolism is influenced by 3 levels of complexity:(1)ancestry groups,(2)sex-smoking subgroups,and(3)presence/absence of poor metabolizer *** 3 groups of variables should determine the maintenance dose and speed of clozapine titration;they are summarised in a table in the *** international clozapine titration guideline recommends measuring CRP levels simultaneously with WBC,at baseline and weekly at least for the first 4 weeks of titration,the highest risk period for clozapine-induced myocarditis.

关键词： titration subgroups absence

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AAV9-mediated Cdk5 inhibitory peptide（CIP） reverses pathological changes and behavioral deficits in the Alzheimer’s disease model mice

AAV9-mediated Cdk5 inhibitory peptide（CIP） reverses pathol...

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中国神经科学学会第十二届全国学术会议

作者： Yong He Suyue Pan Miaojing Xu Rongni He Wei Huang Pingping Song Jianou Huang Han-Ting Zhang Yafang Hu Department of Neurology Nanfang Hospital Southern Medical University Department of Neurology the First People's Hospital of Chenzhou Department of Neurology Zhujiang Hospital Southern Medical University Department of Neurology 421 Hospital departments of behavioral medicine & psychiatry and physiology & pharmacology West Virginia University Health Sciences Center

Cdk5, binding to and activated by p35, phosphorylates multiple substrates and plays an essential role in the development and function of the central neuron system. However, proteolytic production of p25 from p35 under stress conditions leads to inappropriate activation of Cdk5 and contributes to hyperphosphorylation of tau and other substrates related to the pathogenesis of Alzheimer’s disease（AD）. Selective inhibition of aberrant Cdk5 activity via genetic overexpression of Cdk5 inhibitory peptide（CIP） reduces pathological changes and prevents brain atrophy and memory loss in p25-transgenic mice. In the present study, we delivered AAV9-GFP-CIP into brain cells via intracerebroventricular infusion in APP/PSEN1 double transgenic mice at 3-month-old, after the occurrence of β amyloid（Aβ） aggregation and hyperphosphorylation of tau. Three months treatment of AAV9-GFP-CIP reduced pathological changes including tau hyperphosphorylation, Aβ deposit, astrocytosis and microgliosis, which were correlated with the reversal of memory loss and anxiety-like behavior observed in APP/PS1 mice. Neuroprotection effect of AAV9-GFP-CIP lasted to additional seven months, which was the endpoint of the study. These findings provide a novel strategy to selectively targeting Cdk5 for treatment of AD.

关键词： AAV9 Alzheimer’s disease Cdk5 Cdk5 inhibitory peptide(CIP) Tau pathology β amyloid

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Phosphodiesterases:novel targets for treatment of alcoholism

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中国药理学与毒理学杂志 2017年第5期31卷 454-455页

作者： LIU Xin WEN Rui-ting GONG Mei-fang XU Ying Nicolas GRAHAME XU Jiang-ping LIANG Jian-hui Marco CONTI 张汉霆 Institute of pharmacology Taishan Medical University departments of behavioral medicine & psychiatry and physiology & pharmacology Blanchette Rockefeller Neurosciences InstituteWest Virginia University Health Sciences Center Department of Molecular and Cellular pharmacology School of Pharmaceutical SciencesPeking University Department of pharmacology School of Pharmaceutical SciencesSouthern Medical University Department of Pharmaceutical Sciences State University of New York at Buffalo Department of Psychology Indiana University-Purdue University Indianapolis Center for Reproductive Sciences Department of ObstetricsGynecology and Reproductive SciencesUniversity of California 泰山医学院药理学研究所泰山医学院药学院美国西弗吉尼亚大学医学院中国旅美科技协会西弗吉尼亚分会美国西弗吉尼亚华人协会

OBJECTIVE Alcoholism is one of the most damaging psychiatric disorders and causes serious social and health problems in the world. However,there are no ideal treatments for this disease in ***(PDEs) are a superfamily of enzymes consisting of 11 PDE families that hydrolyze cyclicAMP(cA MP) and/or cyclicGMP(cGMP). Among them,PDE4 is critical in the control of intracellular cAMP levels and has been shown to play an important role in the regulation of ethanol ***,the functional role of PDE4 in mediating alcoholism remains unclear. METHODS Ethanol drinking and preference were examined using the two-bottle choice and/or drinking-in-dark(DID) test in high alcohol preferring(HAP) animals,including C57,HAP,and PDE4-subtype knockout mice,and Fawn-Hooded(FH/Wjd) rats,treated with or without the PDE4 inhibitor rolipram or roflumilast. Ethanol withdrawal-induced anxiety-and depressive-like behaviors were examined using the elevated plusmaze,holeboard,forced-swim,and tail-suspension tests in C57 mice or FH rats in the presence of PDE4 inhibition. Levels of cAMP,CREB were determined in brain regions. RESULTS Treatment with rolipram or roflumilast decreased ethanol intake and preference in two-bottle choice and DID tests in C57 and HAP mice as well as FH rats. Mice deficient in PDE4 B,but not PDE4 D,displayed similar effects to general PDE4 inhibition. In addition,rolipram reversed ethanol withdrawal-induced anxietyand depressive-like behaviors 1 d and 14 d,respectively,following withdrawal from ethanol drinking in the two-bottle choice in C57 mice or FH rats. Locomotor activity was not changed in either mice or rats treated with the PDE4 inhibitors. Levels of cAMP,p CREB in the brain were increased by *** The results provide solid evidence for the important role of PDE4 in ethanol consumptionand ethanol withdrawal-induced symptoms. Inhibitors of PDE4,in particular the PDE4 B isoform,can be a novel class of treatment for alcohol

关键词： phosphodiesterase alcohol drinking alcoholism anxiety depression rodents

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Molecular hallmarks of long non-coding RNAs in aging and its significant effect on aging-associated diseases

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Neural Regeneration Research 2023年第5期18卷 959-968页

作者： Syed Aoun Mehmood Sherazi Asim Abbasi Abdullah Jamil Mohammad Uzair Ayesha Ikram Shanzay Qamar Adediji Ayomide Olamide Muhammad Arshad Peter J.Fried Milos Ljubisavljevic Ran Wang Shahid Bashir Department of Biological Sciences Faculty of Basic&Applied SciencesInternational Islamic UniversityIslamabadPakistan Department of Biological Sciences University of ArkansasFayettevilleARUSA Department of pharmacology Government College UniversityFaisalabadPakistan Department of Bioinformatics and Biotechnology Government College UniversityFaisalabadPakistan Department of Chemistry Chulalongkorn UniversityThailand Department of Neurology Berenson-Allen Center for Noninvasive Brain Stimulation and Division of Cognitive NeurologyBeth Israel Deaconess Medical Center(KS 158)Harvard Medical SchoolBostonMAUSA Department of physiology College of Medicine and Health SciencesUnited Arab Emirates UniversityAl AinUnited Arab Emirates Department of psychiatry The First Hospital of Hebei Medical UniversityShijiazhuangHebei ProvinceChina Mental Health Institute of Hebei Medical University ShijiazhuangHebei ProvinceChina Neuroscience Center King Fahad Specialist HospitalDammamSaudi Arabia

Aging is linked to the deterioration of many physical and cognitive abilities and is the leading risk factor for Alzheimer’s disease. The growing aging population is a significant healthcare problem globally that researchers must investigate to better understand the underlying aging processes. Advances in microarrays and sequencing techniques have resulted in deeper analyses of diverse essential genomes(e.g., mouse, human, and rat) and their corresponding cell types, their organ-specific transcriptomes, and the tissue involved in aging. Traditional gene controllers such as DNA-and RNA-binding proteins significantly influence such programs, causing the need to sort out long non-coding RNAs, a new class of powerful gene regulatory elements. However, their functional significance in the aging process and senescence has yet to be investigated and identified. Several recent researchers have associated the initiation and development of senescence and aging in mammals with several well-reported and novel long non-coding RNAs. In this review article, we identified and analyzed the evolving functions of long non-coding RNAs in cellular processes, including cellular senescence, aging, and age-related pathogenesis, which are the major hallmarks of long non-coding RNAs in aging.

关键词： aging Alzheimer’s disease DNA sequence epigenetics immune non-coding RNA oligonucleotides telomere-associated

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behavioral Characteristics of Pharmacologically Selected Lines of Rats: Relevance to Depression

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World Journal of Neuroscience 2014年第3期4卷 225-239页

作者： Darin J. Knapp Lynette C. Daws David H. Overstreet Bowles Center for Alcohol Studies and Department of psychiatry University of North Carolina at Chapel Hill Chapel Hill USA departments of physiology and pharmacology University of Texas Health Science Center at San Antonio San Antonio USA

This brief review discusses the behavioral consequences of two pharmacologically selected lines of rats. Flinders Sensitive (FSL) and Flinders Resistant (FRL) Lines of rats were selected on the basis of differential hypothermic and behavioral responses to the anticholinesterase, diisopropylfluorophosphate (DFP). FSL rats are more sensitive to the hypothermic effects of cholinergic, serotonergic, and dopaminergic agonists but less sensitive to the locomotor or stereotypic effects of dopamine agonists. FSL rats exhibit greater immobility in the forced swim test and reduced social interaction compared with FRL rats, but do not differ in saccharin intake, behavior in the elevated plus maze, or responses for rewarding brain self-stimulation. The exaggerated immobility and reduced social interaction are counteracted by chronic treatment with antidepressants. Because FSL rats were more sensitive to 5-HT1A receptor agonists, high (HDS) and low (LDS) 8-OH-DPATsensitive lines were selectively bred for differential hypothermic responses to the 5-HT1A receptor agonist, 8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT). HDS rats were also more sensitive to the hypothermic effects of oxotremorine, a cholinergic agonist, but selection for this response did not diverge with later selection. HDS rats exhibited greater immobility in the forced swim test than LDS rats and this correlated response could be seen early in selection (generation 3). HDS rats also showed reduced social interaction compared to LDS rats, but did not differ in behavior in the elevated plus maze. These findings confirm that selection for hypothermic responses to pharmacological agents do have behavioral consequences, notably the production of depressive-like phenotypes, which can be counteracted by chronic antidepressant treatment. Because increased 5-HT1A receptor sensitivity was common to both selected lines (FSL and HDS), neurobiological processes dependent on this receptor could contribute to the abnormal

关键词： Diisopropylfluorophosphate (DFP) 8-Hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT) Flinders Sensitive Line (FSL) Flinders Resistant Line (FRL) Rats High and Low 8-OH-DPAT Sensitive (HDS & LDS) Rats Muscarinic Receptors 5-HT1A Receptors Forced Swim Test Social Interaction Test Elevated Plus Maze Depression Anxiety

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Upregulation of PIP3-Dependent Rac Exchanger 1 （P-Rex1）Promotes Prostate Cancer Metastasis

Upregulation of PIP3-Dependent Rac Exchanger 1 （P-Rex1）Pro...

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第十一次中国生物物理学术大会暨第九届全国会员代表大会

作者： Mikio Hoshino Dennis W.Wolff Margaret A.Scofield Frank J.Dowd Department of Biochemistry and Cellular Biology National Institute of NeuroscienceNational Center of Neurology and Psychiatry departments of pharmacology Creighton University School of Medicine

＜正＞Excessive activation of G-protein coupled receptor（GPCR）and receptor tyrosine kinase（RTK）pathways has been linked to prostate cancer *** activation by

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Bis(3)-cognitin inhibits MAO-B and attenuates MPTP toxicity in mice

Bis(3)-cognitin inhibits MAO-B and attenuates MPTP toxicity ...

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中国神经科学学会第十届全国学术会议

作者： Lu YAO Yong LIU Jian LIU Zi-Xu MAO Department of physiology and Pathophysiology Xi'an Jiaotong University College of Medicine Institute of Neurobiology Xi'an Jiaotong University College of Medicine departments of pharmacology and Neurology School of MedicineEmory University

Objective Bis(3)-cognitin(B3C) has previously been shown to provide protection of dopaminergic neurons in a model of Parkinson disease(PD) by reversing myocyte enhancer factor 2D(MEF2D) dysfunction,which is implicated in the pathogenic process of *** the present investigation,we provide evidence that B3C is effective in the MPTP mouse model,not via activation of MEF2D,but through inhibition of MAO-B,the enzyme required to biotransform MPTP to its active neurotoxic metabolite l-methyl-4-phenylpyridinium(MPP).Methods Mice were treated with B3C(1.0 mg /kg/day,i.p,for 10 days) with MPTP(8.0 mg mg /kg/day,i.p,for 10 days) *** were then assessed for motor impairments on rotor and footprint tests and for reductions in TH immunoreactivity in the substantia *** effects of B3C on striatal MPP`+ levels and MAO-B activity were also *** Mice treated with MPTP showed deficits in motor performance,marked a concomitant reduction in TH immunoreactivity in the substantia *** with B3C completely prevented these effects of ***,treatment with B3C also significantly inhibited the MPTP-induced production of striatal MPPand the activity of MAO-B in the *** The neuroprotection observed with B3C pretreatment in the MPTP mouse model was due to the blockade of the conversion of MPTP to its active toxic metabolite MPP,via inhibition of MAO-B.

关键词： Parkinson’s disease bis(3)-cognitin MPTP MAO-B neuroprotection

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