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Predictors of the placebo response in a nutraceutical randomized controlled trial for depression

Journal of Integrative medicine 2024年第1期22卷 46-53页

作者： Rosemary Arnold Jenifer Murphy-Smith Chee H.Ng David Mischoulon Gerard J.Byrne Chad A.Bousman Con Stough Michael Berk Jerome Sarris Professorial Unit the Melbourne ClinicDepartment of PsychiatryUniversity of MelbourneRichmond 3121Australia Depression Clinical and Research Program Department of PsychiatryMassachusetts General HospitalHarvard Medical SchoolBostonMA 02115USA Faculty of medicine Discipline of PsychiatryCentre for Clinical ResearchRoyal Brisbane&Women’s HospitalHerstonthe University of QueenslandBrisbane 4006Australia departments of Medical Genetics PsychiatryPhysiology&Pharmacology and Community Health SciencesUniversity of CalgaryCalgaryAB T2N 1N4Canada Department of psychiatry the University of MelbourneMelbourne 3052Australia Centre for Human Psychopharmacology Swinburne UniversityMelbourne 3122Australia The Institute for Mental and Physical Health and Clinical Translation School of MedicineBarwon HealthDeakin UniversityGeelong 3220Australia The Centre of Excellence in Youth Mental Health the University of MelbourneParkville 3052Australia Florey Institute of Neuroscience and Mental Health the University of MelbourneParkville 3052Australia NICM Health Research Institute Western Sydney UniversityWestmeadNSW 2145Australia

Objective The placebo response in depression studies is the change in symptoms amongst those who receive an inactive treatment.Many well-designed randomized controlled trials(RCTs)of depression have a high proportion of placebo responders,with little understanding as to why.The present study assesses characteristics associated with the placebo response in a nutraceutical trial with a large proportion of placebo responders.Methods This is a secondary analysis of a nutraceutical depression RCT which identified no overall treatment benefit relative to placebo(n=69 in placebo group).We investigated participant characteristics such as socio-demographics,clinical features,and recruitment methods,and their association with the placebo response.Monoaminergic genetic polymorphisms were also assessed.Placebo response was measured based on change in Montgomery-Asberg Depression Rating Scale score.The association of these hypothesis-driven variables of interest and the placebo response was examined using linear mixed effects models.Results Greater levels of education,particularly pursuing post-high school education,better self-reported general health,marriage/de facto,greater improvement in the first trial week,and more failed antidepressant therapies in the current depressive episode were associated with greater placebo response.An increased placebo response was not found in those recruited via social media nor in those with concomitant antidepressant therapy.Single nucleotide polymorphisms from the tryptophan hydroxylase 1(TPH1)gene(A779C and A218C)were weakly associated with greater placebo response,although the evidence was attenuated after accounting for multiple comparisons.Conclusion This is,to our knowledge,the first study within nutraceutical research for depression to assess the association between participant characteristics and variation in the placebo response.Several variables appeared to predict the placebo response.Such findings may encourage future trial designs which could dampen placebo response,improve as

关键词： Randomized controlled trial Placebo Depression Nutraceutical psychiatry

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Dysregulated microRNAs in type 2 diabetes and breast cancer:Potential associated molecular mechanisms

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World Journal of Diabetes 2024年第6期15卷 1187-1198页

作者： Alex Cleber Improta-Caria Filipe Ferrari João Lucas Penteado Gomes Paloma Brasilio Villalta Úrsula Paula RenóSoci Ricardo Stein Edilamar M Oliveira Laboratory of Biochemistry and Molecular Biology of the Exercise Physical Education and Sport SchoolUniversity of São PauloSão Paulo 05508-030Brazil Graduate Program in Cardiology and Cardiovascular Sciences Federal University of Rio Grande do SulHospital de Clínicas de Porto AlegrePorto Alegre 90035003Brazil Laboratory of Metabolic Disorders(Labdime) School of Applied SciencesUniversity of Campinas-UNICAMPCampinas 13484-350Brazil departments of Internal medicine Molecular Pharmacology and PhysiologyCenter for Regenerative MedicineUSF Health Heart InstituteMorsani College of MedicineUniversity of South FloridaTampaFL 33602United States

Type 2 diabetes(T2D)is a multifaceted and heterogeneous syndrome associated with complications such as hypertension,coronary artery disease,and notably,breast cancer(BC).The connection between T2D and BC is established through processes that involve insulin resistance,inflammation and other factors.Despite this comprehension the specific cellular and molecular mechanisms linking T2D to BC,especially through microRNAs(miRNAs),remain elusive.miRNAs are regulators of gene expression at the post-transcriptional level and have the function of regulating target genes by modulating various signaling pathways and biological processes.However,the signaling pathways and biological processes regulated by miRNAs that are associated with T2D and BC have not yet been elucidated.This review aims to identify dysregulated miRNAs in both T2D and BC,exploring potential signaling pathways and biological processes that collectively contribute to the development of BC.

关键词： Type 2 diabetes Breast cancer MicroRNAs Molecular mechanisms

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Zataria multiflora and its constituent,carvacrol,counteract sepsis-induced aortic and cardiac toxicity in rat:Involvement of nitric oxide and oxidative stress

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Animal Models and Experimental medicine 2023年第3期6卷 221-229页

作者： Mahmoud Hosseini Zohreh Arab Farimah Beheshti Akbar Anaeigoudari Farzaneh Shakeri Arezoo Rajabian psychiatry and behavioral Sciences Research Center Mashhad University of Medical SciencesMashhadIran Applied Biomedical Research Center Mashhad University of Medical SciencesMashhadIran Neuroscience Research Center Torbat Heydariyeh University of Medical SciencesTorbat HeydariyehIran Department of physiology School of Paramedical SciencesTorbat Heydariyeh University of Medical SciencesTorbat HeydariyehIran Department of physiology School of MedicineJiroft University of Medical SciencesJiroftIran Natural Products and Medicinal Plants Research Center North Khorasan University of Medical SciencesBojnurdIran Department of physiology and pharmacology School of MedicineNorth Khorasan University of Medical SciencesBojnurdIran Department of Internal medicine Faculty of MedicineMashhad University of Medical SciencesMashhadIran

Background:Zataria multiflora and carvacrol showed various pharmacological prop-erties including anti-inflammatory and anti-oxidant effects.However,up to now no studies have explored its potential benefits in ameliorating sepsis-induced aortic and cardiac injury.Thus,this study aimed to investigate the effects of Z.multiflora and carvacrol on nitric oxide(NO)and oxidative stress indicators in lipopolysaccharide(LPS)-induced aortic and cardiac injury.Methods:Adult male Wistar rats were assigned to:Control,lipopolysaccharide(LPS)(1 mg/kg,intraperitoneal(i.p.)),and Z.multiflora hydro-ethanolic extract(ZME,50–200 mg/kg,oral)-and carvacrol(25–100 mg/kg,oral)-treated groups.LPS was in-jected daily for 14 days.Treatment with ZME and carvacrol started 3 days before LPS administration and treatment continued during LPS administration.At the end of the study,the levels of malondialdehyde(MDA),NO,thiols,and antioxidant enzymes were evaluated.Results:Our findings showed a significant reduction in the levels of superoxide dis-mutase(SOD),catalase(CAT),and thiols in the LPS group,which were restored by ZME and carvacrol.Furthermore,ZME and carvacrol decreased MDA and NO in car-diac and aortic tissues of LPS-injected rats.Conclusions:The results suggest protective effects of ZME and carvacrol on LPS-induced cardiovascular injury via improved redox hemostasis and attenuated NO pro-duction.However,additional studies are needed to elucidate the effects of ZME and its constituents on inflammatory responses mediated by LPS.

关键词： carvacrol lipopolysaccharide nitric oxide oxidative injury sepsis Z.multiflora

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Brucine N-oxide reduces ethanol intake and preference in alcohol-preferring Fawn-Hooded rats

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中国药理学与毒理学杂志 2017年第5期31卷 479-480页

作者： LIANG Jian-hui WEI Shou-peng LI Yu-ling GONG Qi WANG Yan-ting LIANG Hui LIU Qing ZHANG Han-ting CHEN Feng Andrew J LOWRENCE Department of Molecular and Cellular pharmacology School of Pharmaceutical Sciences Department of pharmacology School of Basic Medicine SciencesPeking University Institute of Psycopharmacology Central Institute of Mental HealthUniversity of Heidelberg departments of behavioral medicine & psychiatry and physiology& pharmacology West Virginia University Health Sciences Center The Florey Institute of Neuroscience and Mental Health University of Melbourne

OBJECTIVE The alcoholism-related social problems have burdened the public health heavily.A better therapy for alcohol dependence as a chronic brain disease is highly required and interests the scientists worldwide. Our group has focused on screening the right drug with low toxicity and a sound curative effect from traditional Chinese medicine. METHODS Alcohol-preferring Fawn-Hooded(FH/Wjd) rat was used as an animal model of alcoholism to evaluate the effects of brucine N-oxide(BNO),an alkoloid naturally existing in the seeds of Strychnos nux-vomica L,on the alcohol-drinking behaviors.Furthermore,its adverse action and toxicity were investigated. RESULTS Treatment with BNO at the doses of 30,50 and 70 mg · kg^(-1)reduced the voluntary alcohol consumption and preference dosedependently and selectively without altering their water intake,total fluid intake,food consumption,body weight as well as sucrose preference. Remarkably,70 mg·kg^(-1)of BNO did suppress the deprivationinduced elevation of alcohol ingestion. Moreover,BNO used at the same doses as above had no influence on locomotion in an open field test and could not result in the place preference effect. CONCLUSION Taken together,BNO is of some significant pharmacological profiles to inhibit symptoms of alcohol dependence with high safety,and thence may be a potential pharmacotherapy.

关键词： brucine N-oxide ethanol

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Ryanodine receptors as pharmacological targets for heart disease

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Acta Pharmacologica Sinica 2007年第7期28卷 937-944页

作者： Marco SANTONASTAS Xander H T WEHRENS departments of Molecular physiology and Biophysics departments of Molecular physiology and Biophysics and Medieine(Cardiology) Baylor College of MedicineHoustonTexas 77030USA

Calcium release from intracellular stores plays an important role in the regulationof muscle contraction and electrical signals that determine the heart rhythm.Theryanodine receptor （RyR） is the major calcium (Ca2+) release channel required forexcitation-contraction coupling in the heart.Recent studies have demonstratedthat RyR are macromolecular complexes comprising of 4 pore-forming channelsubunits,each of which is associated with regulatory subunits.Clinical andexperimental studies over the past 5 years have provided compelling evidencethat intracellular Ca2+release channels play a pivotal role in the development ofcardiac arrhythmias and heart failure.Changes in the channel regulation andsubunit composition are believed to cause diastolic calcium leakage from thesarcoplasmic reticulum,which could trigger arrhythmias and weaken cardiaccontractility.Therefore,cardiac RyR have emerged as potential therapeutic tar-gets for the treatment of heart disease.Consequently,there is a strong desire toidentify and/or develop novel pharmacological agents that may target these Ca2+signaling pathways.Pharmacological agents known to modulate RyR in the heart,and their potential application towards the treatment of heart disease are dis-cussed in this review.

关键词： arrhythmias calcium release channel heart failure pharmacology ryanodine receptor

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Targeting neuroinflammation in Alzheimer's disease:from mechanisms to clinical applications

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Neural Regeneration Research 2023年第4期18卷 708-715页

作者： Zi-Zhen Si Chen-Jun Zou Xi Mei Xiao-Fang Li Hu Luo Yao Shen Jun Hu Xing-Xing Li Lun Wu Yu Liu Pharmacy Department The Affiliated Hospital of Medical SchoolNingbo UniversityNingboZhejiang ProvinceChina Department of physiology and pharmacology School of MedicineNingbo UniversityNingboZhejiang ProvinceChina Department of Geriatric psychiatry Ningbo Kangning HospitalNingboZhejiang ProvinceChina Key Laboratory Office of Sleep medicine Ningbo Kangning HospitalNingboZhejiang ProvinceChina Department of Psychology Collage of Teacher EducationNingbo UniversityNingboZhejiang ProvinceChina Department of Preventive medicine School of MedicineNingbo UniversityNingboZhejiang ProvinceChina

Alzheimer’s disease is characterized by sustained neuroinflammation leading to memory loss and cognitive decline.The past decade has witnessed tremendous efforts in Alzheimer’s disease research;however,no effective treatment is available to prevent disease progression.An increasing body of evidence suggests that neuroinflammation plays an important role in Alzheimer’s disease pathogenesis,alongside the classical pathological hallmarks such as misfolded and aggregated proteins(e.g.,amyloid-beta and tau).Firstly,this review summarized the clinical and pathological characteristics of Alzheimer’s disease.Secondly,we outlined key aspects of glial cell-associated inflammation in Alzheimer’s disease pathogenesis and provided the latest evidence on the roles of microglia and astrocytes in Alzheimer’s disease pathology.Then,we revealed the double-edged nature of inflammatory cytokines and inflammasomes in Alzheimer’s disease.In addition,the potential therapeutic roles of innate immunity and neuroinflammation for Alzheimer’s disease were also discussed through these mechanisms.In the final section,the remaining key problems according to the current research status were discussed.

关键词： Alzheimer’s disease astrocytes immune signaling inflammatory cytokines microglia neuroinflammation neurotoxicity therapeutic strategies

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Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy

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Neuroscience Bulletin 2012年第6期28卷 729-736页

作者： Bijan Akbarpour Mohammad Sayyah Vahab Babapour Reza Mahdian Siamak Beheshti Ahmad Reza Kamyab departments of physiology and pharmacology Pasteur Institute of Iran.Tehran 131694-3551Islamic Republic of Iran Department of physiology Faculty of Veterinary MedicineIslamic Azad UniversityScience and Research BranchTehran 14778-93855Islamic Republic of Iran departments of physiology and pharmacology Pasteur Institute of IranTehran 131694-3551Islamic Republic of Iran Department of physiology Faculty of Veterinary MedicineTehran UniversityTehran 141996-31111Islamic-Republic of Iran Department of Molecular medicine Biotechnology Research CenterPasteur Institute of Iran Department of Biology Faculty of Science University of IsfahanIsfahan 81746-73441Islamic Republic of Iran

Objective Understanding the molecular and cellular mechanisms underlying epileptogenesis yields new in- sights into potential therapies that may ultimately prevent epilepsy. Gap junctions （GJs） create direct intercellular conduits between adjacent cells and are formed by hexameric protein subunits called connexins （Cxs）. Changes in the expression of Cxs affect GJ communication and thereby could modulate the dissemination of electrical discharges. The hippocampus is one of the main regions involved in epileptogenesis and has a wide network of GJs between different cell types where Cx30 is expressed in astrocytes and Cx32 exists in neurons and oligodendrocytes. In the present study, we evaluated the changes of Cx30 and Cx32 expression in rat hippocampus during kindling epileptogenesis. Methods Rats were stereotaxically implanted with stimulating and recording electrodes in the basolateral amygdala, which was electrically stimulated once daily at afterdischarge threshold. Expression of Cx30 and Cx32, at both the mRNA and protein levels, was measured in the hippocampus at the beginning, in the middle （after acquisition of focal seizures）, and at the end （after establishment of generalized seizures） of the kindling process, by real-time PCR and Western blot. Results Cx30 mRNA expression was upregulated at the beginning of kindling and after acquisition of focal seizures. Then it was downregulated when the animals acquired generalized seizures. Overexpression of Cx30 mRNA at the start of kindling was consistent with the respective initial protein increase. Thereafter, no change was found in protein abundance during kindling. Regarding Cx32, mRNA expression decreased after acquisition of generalized seizures and no other significant change was detected in mRNA and protein abundance during kindling. Conclusion We speculate that Cx32 GJ communication in the hip- pocampus does not contribute to kindling epileptogenesis. The Cx30 astrocytic network localized to perivascular regions in the hippocampus is, however, overexpres

关键词： connexin 30 connexin 32 hippocampus kindling

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Animal models of Huntington's disease: implications in uncovering pathogenic mechanisms and developing therapies

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Acta Pharmacologica Sinica 2006年第10期27卷 1287-1302页

作者： Lin-hui WANG~2 Zheng-hong QIN~(3,4) departments of ~2physiology and ~3pharmacology,Soochow University School of medicine,Suzhou 215123,China Department of physiology Soochow University School of Medicine Suzhou China Department of pharmacology Soochow University School of Medicine Suzhou China

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder,which is caused by an abnormal expansion of Cytosine Adenine Guanine (CAG)trinucleotide repeat in the gene making huntingtin (Htt).Despite intensiveresearch efforts devoted to investigate molecular mechanisms of pathogenesis,effective therapy for this devastating disease is still not available at present.Thedevelopment of various animal models of HD has offered alternative approachesin the study of HD molecular pathology.Many HD models,including chemical-induced models and genetic models,mimic some aspects of HD symptoms andpathology.To date,however,there is no ideal model which replicates all of theessential features of neuropathology and progressive motor and cognitive impair-ments of human HD.As a result,our understanding of molecular mechanisms ofpathogenesis in HD is still limited.A new model is needed in order to uncover thepathogenesis and to develop novel therapies for HD.In this review we discussedusefulness and limitations of various animal and cellular models of HD in uncov-ering molecular mechanisms of pathogenesis and developing novel therapies forHD.

关键词： Huntington’s disease huntingtin neurodegeneration animal models

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Deconstructing brain-derived neurotrophic factor actions in adult brain circuits to bridge an existing informational gap in neuro-cell biology

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Neural Regeneration Research 2016年第3期11卷 363-367页

作者： Heather Bowling Aditi Bhattacharya Eric Klann Moses V.Chao Center for Neural Science New York University Center for Brain Development and Repair Institute for Stem Cell Biology and Regenerative Medicine departments of Cell Biology Physiologyand Neuroscience and PsychiatryKimmel Center for Biology and Medicine at the Skirball InstituteNew York University School of Medicine

Brain-derived neurotrophic factor（BDNF） plays an important role in neurodevelopment,synaptic plasticity,learning and memory,and in preventing neurodegeneration.Despite decades of investigations into downstream signaling cascades and changes in cellular processes,the mechanisms of how BDNF reshapes circuits in vivo remain unclear.This informational gap partly arises from the fact that the bulk of studies into the molecular actions of BDNF have been performed in dissociated neuronal cultures,while the majority of studies on synaptic plasticity,learning and memory were performed in acute brain slices or in vivo.A recent study by Bowling-Bhattacharya et al.,measured the proteomic changes in acute adult hippocampal slices following treatment and reported changes in proteins of neuronal and non-neuronal origin that may in concert modulate synaptic release and secretion in the slice.In this paper,we place these findings into the context of existing literature and discuss how they impact our understanding of how BDNF can reshape the brain.

关键词： BONLAC BDNF adult slice proteomics neuroproteomics SILAC BONCAT hippocampus proteinsynthesis

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Control of de novo root regeneration efficiency by developmental status of Arabidopsis leaf explants

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Journal of Genetics and Genomics 2019年第3期46卷 133-140页

作者： Jing Pan Fei Zhao Guifang Zhang Yu Pan Lijun Sun Ning Bao Peng Qin Lyuqin Chen Jie Yu Yijing Zhang Lin Xu National Key Laboratory of Plant Molecular Genetics CAS Center for Excellence in Molecular Plant Sciences Shanghai Institute of Plant Physiology and Ecology Chinese Academy of Sciences University of Chinese Academy of Sciences School of Life Sciences Nantong University School of Public Health Nantong University Department of Instrument Science and Engineering Shanghai Jiao Tong University departments of Neurosurgery Psychiatry and Behavioral Sci-ences Stanford University School of Medicine

De novo root regeneration(DNRR) has wide applications in agriculture such as those related to cutting technology. Detached Arabidopsis thaliana leaf explants can regenerate adventitious roots without added hormones. The regenerative ability is highly dependent on the developmental status of the leaf. An immature leaf has a higher regenerative ability, while a mature leaf is difficult to regenerate. Using RNASeq analysis, we showed that the expression levels of many genes, including those in the auxin network,changed during leaf maturation. Particularly, the expression levels of many YUCCA(YUC) genes in the auxin biosynthesis pathway are responsive to leaf maturation. Overexpression of YUC1 in the yuc-1 D dominant mutant rescued the rooting defects caused by leaf maturation. In addition, YUC4 expression levels were also affected by circadian rhythms. The regenerative ability was reduced in both immature and mature mutant leaf explants from the new wuschel-related homeobox 11-3(wox11-3) and wox12-3 mutant alleles created by the CRISPR/Cas9 method. Overall, the transcriptome and genetic data, together with the auxin concentration analysis, indicate that the ability to upregulate auxin levels upon detachment may be reduced during leaf maturation. Thus, multiple developmental and environmental signals may converge to control auxin accumulation, which affects the efficiency of the WOX11/12-mediated DNRR from leaf explants.

关键词： De novo root regeneration WOX11 Arabidopsis Developmental status Circadian rhythms YUCCA

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