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p66Shc-mediated oxidative stress is involved in gestational diabetes mellitus

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World Journal of Diabetes 2021年第11期12卷 1894-1907页

作者： Ting-Ting Huang Wen-Juan Sun Hai-Ying Liu Hong-Li Ma Bao-Xia Cui Cheeloo College of Medicine Shandong UniversityJinan 250000Shandong ProvinceChina Department of Obstetrics Taian City Central HospitalTaian 271000Shandong ProvinceChina Department of Obstetrics The Second HospitalCheeloo College of MedicineShandong UniversityJinan 250000Shandong ProvinceChina Department of Obstetrics and Gynecology Qilu Hospital(Qingdao)Cheeloo College of MedicineShandong UniversityQingdao 266000Shandong ProvinceChina Department of Obstetrics and Gynecology Qilu HospitalCheeloo College of MedicineShandong UniversityJinan 250013Shandong ProvinceChina

BACKGROUND Gestational diabetes mellitus(GDM)is associated with a heightened level of oxidative stress,which is characterized by the overproduction of reactive oxygen species(ROS)from *** studies showed that mitochondrial dysfunction is regulated by dynamin-related protein 1(Drp1)and p66Shc in *** The aim was to investigate the expression of Drp1 and p66Shc and their possible mechanisms in the pathogenesis of *** A total of 30 pregnant women,15 with GDM and 15 without GDM,were *** blood mononuclear cells and placental tissue were *** human JEG3 trophoblast cell line was cultivated in 5.5 mmol/L or 30 mmol/L glucose and transfected with wild-type(wt)-p66Shc and p66Shc siRNA.P66Shc and Drp1 mRNA levels were detected by quantitative real-time polymerase chain *** expression of p66Shc and Drp1 was assayed by immunohistochemistry and western *** was assayed by dihydroethidium *** The p66Shc mRNA level was increased in the serum(Pmitochondrial fusion-fission balance could be a novel strategy for GDM treatment.

关键词： p66Shc Dynamin-related protein 1 Gestational diabetes mellitus Oxidative stress mitochondrial dysfunction

Thiamine deficiency perturbed energy metabolism enzymes in brain mitochondrial fraction of Swiss mice

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Frontiers in Biology 2017年第4期12卷 290-297页

作者： Anupama Sharma Renu Bist Surender Singh Department of Bioscience and Biotechnology Banasthali University BanasthaIL Rajasthan lndia Animal Biotechnology Centre National Dairy Research Institute Karnal India

BACKGROUND： Thiamine is an essential cofactor associated with several enzymes in energy metabolism and its deficiency may lead to neurological deficits. Current research evaluated the biochemical and molecular changes in TCA cycle enzymes using the mitochondrial fraction of the brain following thiamine deficiency （TD） in mice. METHODS： The investigation was carried out on Swiss mice （6-8 week old） allocated into three groups. First group was control; second and third group were made thiamine deficient for 8 and 10 days. RESULTS： Current study showed that alpha-ketoglutarate dehydrogenase （KGDHC）（thiamine-dependent enzyme） level found to be significantly reduced in experimental groups as compared to control group. In comparison to control group, a significant decrease in the succinate dehydrogenase （SDH） activity was calculated in group II and group III （p 〈 0.0001） mice. Diminished enzymatic activity of fumarase and MDH enzyme in thiamine deficient groups exposed for 8 and 10 days was calculated as compared to control group. The expression analysis of different genes governing TCA cycle enzymes in different experimental groups showed that there was a negotiable change in the expression of fumarase and DLD （dihydrolipoyl dehydrogenase- E3 subunit of KGDHC） whereas a declined in the expression of SDH and two subunits of KGDHC i.e. OGDH （2-oxoglutarate dehydrogenase- E1 subunit of KGDHC） and DLST （dihydrolipoyllysine-residue succinyltransferase- E2 subunit of KGDHC） was observed as compared to control group. CONCLUSIONS： Hence, current findings strongly entail that TD promotes alteration in energy metabolism in brain mitochondria which will decline the neuronal progression which may lead to neurodegenerative diseases such as Alzheimer＇s diseases.

关键词： thiamine brain TCA cycle enzymes mitochondrial dysfunction

Development and progression of cancer cachexia:Perspectives from bench to bedside

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Sports Medicine and Health Science 2020年第4期2卷 177-185页

作者： Seongkyun Lim Jacob L.Brown Tyrone A.Washington Nicholas P.Greene Cachexia Research Laboratory Exercise Science Research CenterDepartment of Human Health Performance and RecreationUniversity of Arkansas155 Stadium DrFayettevilleARUSA Aging and Metabolism Research Program Oklahoma Medical Research Foundation825 NE 13th StOklahoma CityOKUSA Exercise Muscle Biology Laboratory Exercise Science Research CenterDepartment of Human Health Performance and RecreationUniversity of Arkansas155 Stadium DrFayettevilleARUSA

Cancer cachexia(CC)is a devastating syndrome characterized by weight loss,reduced fat mass and muscle mass that affects approximately 80%of cancer patients and is responsible for 22%-30%of cancer-associated *** underlying mechanisms for the development of CC are crucial to advance therapies to treat CC and improve cancer *** is a multi-organ syndrome that results in extensive skeletal muscle and adipose tissue wasting;however,CC can impair other organs such as the liver,heart,brain,and bone as well.A considerable amount of CC research focuses on changes that occur within the muscle,but cancer-related impairments in other organ systems are ***,metabolic changes in organ systems other than muscle may contribute to ***,the purpose of this review is to address degenerative mechanisms which occur during CC from a whole-body *** the information known about metabolic changes that occur in response to cancer is necessary to develop and enhance therapies to treat *** much of the current evidences in CC are from pre-clinical models we should note the majority of the data reviewed here are from preclinical models.

关键词： Muscle atrophy Tumor-bearing mouse Lewis lung carcinoma Protein turnover mitochondrial dysfunction

Septic cardiomyopathy:characteristics,evaluation,and mechanism

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Emergency and Critical Care Medicine 2022年第3期2卷 135-147页

作者： Wanlin Xue Jiaojiao Pang Jiao Liu Hao Wang Haipeng Guo Yuguo Chen Department of Critical Care Medicine Qilu Hospital of Shandong UniversityJinanShandongChina The Key Laboratory of Emergency and Critical Care Medicine of Shandong Province Qilu Hospital of Shandong UniversityJinanShandongChina The Key Laboratory of Cardiovascular Remodeling and Function Research Chinese Ministry of Education and Chinese Ministry of HealthQilu Hospital of Shandong UniversityJinanShandongChina Department of Emergency Medicine and Chest Pain Center Qilu Hospital of Shandong UniversityJinanShandongChina Department of Critical Care Medicine Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghaiChina

Sepsis is a common clinical disease;if there is no early active treatment,it is likely to develop into multiple organ dysfunction syndrome and even cause *** cardiomyopathy is a complication of sepsis-related cardiovascular failure,characterized by reversible left ventricular dilatation and decreased ventricular systolic and/or diastolic *** present,echocardiography and biomarkers are often used to screen septic cardiomyopathy in *** there is still a lack of clear diagnostic criteria for septic cardiomyopathy,according to existing studies,the pathogenesis of several septic cardiomyopathy has been clarified,such as immune response caused by infection and mitochondrial *** review summarizes the characteristics,pathophysiology,and diagnosis of septic cardiomyopathy and focuses on the mechanisms of infection immunity and mitochondrial dysfunction.

关键词： Echocardiography Infection immunity mitochondrial dysfunction Sepsis-induced cardiomyopathy Septic cardiomyopathy

Sodium-glucose cotransporter-2 inhibitors protect tissues via cellular and mitochondrial pathways:Experimental and clinical evidence

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World Journal of Experimental Medicine 2024年第2期14卷 46-52页

作者： Raúl Lelio Sanz Sebastián García Menéndez Felipe Inserra Leon Ferder Walter Manucha Department of Pathology Facultad de Ciencias MédicasUniversidad Nacional de CuyoMendoza 5500Argentina Department of Pharmacology Instituto de Medicina y Biología Experimental de CuyoCentro Científico TecnológicoMendoza 5500Argentina Department of Nephrology Universidad de MaimónidesCiudad Autónoma de Buenos Aires C1405Argentina Department of Cardiology Universidad de MaimónidesCiudad Autónoma de Buenos Aires C1405Argentina

mitochondrial dysfunction is a key driver of cardiovascular disease(CVD)in metabolic syndrome and *** dysfunction promotes the production of reactive oxygen species(ROS),which cause oxidative stress and *** II,the main mediator of the renin-angiotensin-aldosterone system,also contributes to CVD by promoting ROS *** activity of sirtuins(SIRTs),a family of proteins that regulate cellular metabolism,also worsens oxidative *** of energy production by mitochondria is a common feature of all metabolic *** SIRT levels and 5’adenosine monophosphate-activated protein kinase signaling stimulate hypoxia-inducible factor 1 beta,which promotes ***,in turn,increases autophagy and mitophagy,processes that clear cells of debris and protect against *** cotransporter-2 inhibitors(SGLT2i),a class of drugs used to treat type 2 diabetes,have a beneficial effect on these *** clinical trials have shown that SGLT2i improves cardiac function and reduces the rate of cardiovascular and renal ***2i also increase mitochondrial efficiency,reduce oxidative stress and inflammation,and strengthen *** findings suggest that SGLT2i hold great potential for the treatment of ***,they are proposed as anti-aging drugs;however,rigorous research is needed to validate these preliminary findings.

关键词： Sodium-glucose cotransporter-2 inhibitors Cardiovascular diseases Sirtuins Oxidative stress Inflammation mitochondrial dysfunction

An Animal Model of Sudden Onset Sensorineural Hearing Loss with Vestibular Function Disturbances Induced By mitochondrial Toxin

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Journal of Otology 2006年第2期1卷 86-93页

作者： PYYKK Ilmari Department of Otolaryngology Tampere University HospitalTeiskontie 3533520 TampereFinland (J.Z.I.P.)

Objective To establish an animal model of sudden onset sensorineural hearing loss (SSNHL) to study its mechanisms. Materials and methods The inner ear was exposed to 3-nitropropionic acid at 0.5 mol/L (3-NP (H)) and 0.3 mol/L (3-NP (L)) through the round window membrane for 30 minutes in 50 male guinea pigs. Thresholds of auditory brainstem responses(ABR) were established before the treatment and retested at 4 hours, 1 day, 3 days and 6 days following 3-NP exposure. Control animals were treated with phosphate buffered saline (PBS) and their ABRs were retested at 4 hours and 1 day after the treatment. Animals were monitored for nystagmus and postural signs of vestibular dysfunction, using a digital video camera, following the treatment procedure. Specimens were taken at 12 hours, 1 day, 3 days and 7 days following 3-NP(H) exposure and embedded in JB4 for light microscopy observation. Results ABRs were lost in all animals tested at 4 hours following 3-NP (H) exposure. The rate of complete ABR loss decreased as post-treatment test time increased. ABRs were lost in 80% (4/5) of the animals at 1 day after exposure to 3-NP (L). Spontaneous horizontal nystagmus with a fast phase away from the treated ear developed in all 3-NP (H)-treated animals and in 20 % ( 1/5) of the animals exposed to 3-NP (L), except for the one treated bilaterally. Various degree of postural disturbances consistent with unilateral vestibular dysfunction, such as spontaneous barrel rolling towards the exposure side while walking, were seen in all animals exposed to 3-NP(H) and 40% (2/5) of animals exposed to 3-NP(L), except for the one animal treated bilaterally, which showed no signs of imbalance. Both nystagmus and postural disturbances resolved in 2 days following 3-NP exposure. Histological study showed temporary edema tin the organ or Corti, Claudius cells and the inner sulcus cells 3 days after 3-NP (H) treatment. Enlargement of intercellular space in the spiral prominence was first noticed at

关键词： Hearing loss vertigo mitochondrial dysfunction animal model histology

Metabolomic changes in children with autism

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World Journal of Clinical Pediatrics 2024年第2期13卷 171-197页

作者： Mohammed Al-Beltagi Nermin Kamal Saeed Adel Salah Bediwy Reem Elbeltagi Department of Pediatric Faculty of MedicineTanta UniversityTanta 31511AlghrabiaEgypt Department of Pediatric University Medical CenterKing Abdulla Medical CityArabian Gulf UniversityManama 26671Bahrain Department of Pediatric University Medical CenterDr.Sulaiman Al Habib Medical GroupManamaBahrainManama 26671Bahrain Medical Microbiology Section Department of PathologySalmaniya Medical ComplexMinistry of HealthKingdom of BahrainManama 12Bahrain Medical Microbiology Section Department of PathologyIrish Royal College of SurgeonBahrainBusaiteen 15503MuharraqBahrain Department of Pulmonology Faculty of MedicineTanta UniversityTanta 31527AlghrabiaEgypt Department of Chest Disease University Medical CenterKing Abdulla Medical CityArabian Gulf UniversityManama 26671Bahrain Department of Chest Disease University Medical CenterDr.Sulaiman Al Habib Medical GroupManamaManama 26671Bahrain Department of Medicine The Royal College of Surgeons in Ireland-BahrainBusiateen 15503MuharraqBahrain

BACKGROUND Autism spectrum disorder(ASD)is a neurodevelopmental condition characterized by deficits in social communication and repetitive *** profiling has emerged as a valuable tool for understanding the underlying metabolic dysregulations associated with *** To comprehensively explore metabolomic changes in children with ASD,integrating findings from various research articles,reviews,systematic reviews,meta-analyses,case reports,editorials,and a book *** A systematic search was conducted in electronic databases,including PubMed,PubMed Central,Cochrane Library,Embase,Web of Science,CINAHL,Scopus,LISA,and NLM catalog up until January *** criteria encompassed research articles(83),review articles(145),meta-analyses(6),systematic reviews(6),case reports(2),editorials(2),and a book chapter(1)related to metabolomic changes in children with *** criteria were applied to ensure the relevance and quality of included *** The systematic review identified specific metabolites and metabolic pathways showing consistent differences in children with ASD compared to typically developing *** metabolic biomarkers may serve as objective measures to support clinical assessments,improve diagnostic accuracy,and inform personalized treatment *** profiling also offers insights into the metabolic alterations associated with comorbid conditions commonly observed in individuals with *** Integration of metabolomic changes in children with ASD holds promise for enhancing diagnostic accuracy,guiding personalized treatment approaches,monitoring treatment response,and improving *** research is needed to validate findings,establish standardized protocols,and overcome technical challenges in metabolomic *** advancing our understanding of metabolic dysregulations in ASD,clinicians can improve the lives of affected individuals and their families.

关键词： Autism spectrum disorder Metabolic dysregulations Metabolomic changes Children mitochondrial dysfunction Oxidative stress Amino acids

mitochondrial damage and biogenesis in acetaminophen-induced liver injury

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Liver Research 2019年第3期3卷 150-156页

作者： Hartmut Jaeschke Luqi Duan Nga T.Nguyen Anup Ramachandran Department of Pharmacology Toxicology&TherapeuticsUniversity of Kansas Medical CenterKansas CityKSUSA

Liver injury and acute liver failure caused by acetaminophen(APAP)overdose is the clinically most important drug toxicity in Western *** investigations have revealed a central role of mitochondria in the *** formation of the reactive metabolite N-acetyl-p-benzoquinone imine(NAPQI)after an overdose leads to hepatic glutathione depletion,mitochondrial protein adducts formation and an initial oxidant stress,which triggers the activation of mitogen activated protein(MAP)kinase cascade ultimately leading to c-jun N-terminal kinase(JNK)***-JNK translocates to the mitochondria and amplifies the oxidative and nitrosative stress eventually causing the mitochondrial membrane permeability transition pore opening and cessation of adenosine triphosphate(ATP)*** addition,mitochondrial matrix swelling ruptures the outer membrane and releases endonucleases,which cause nuclear deoxyribonucleic acid(DNA)***,the nuclear DNA damage and the extensive mitochondrial dysfunction result in necrotic cell ***,the procell death signaling events are counteracted by adaptive responses such as autophagy and mitochondrial *** improved mechanistic insight into the pathophysiology leads to better understanding of the mechanisms of action of the existing antidote N-acetylcysteine and justifies the clinical testing of novel therapeutics such as 4-methylpyrazole and calmangafodipir.

关键词： Acetaminophen(APAP)hepatotoxicity mitochondrial dysfunction Biogenesis Oxidant stress Peroxynitrite c-Jun N-terminal kinase(JNK)

Optical monitoring of tissue viability parameters in vivo: from experimental animals to clinical applications

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Frontiers of Optoelectronics 2010年第2期3卷 153-162页

作者： Avraham MAYEVSKY Efrat BARBIRO-MICHAELY Mina and Everard Goodman Faculty of Life Sciences Gonda Brain Research Center Bar-Ilan University Criti Sense Ltd.

Optical monitoring of tissue physiological and biochemical parameters in real-time is a new approach and a powerful tool for better clinical diagnosis and *** of the devices available for monitoring patients in critical conditions provide information on body respiratory and hemodynamic ***,monitoring of patients at the cellular and tissue level is very *** monitoring of mitochondrial nicotinamide adenine dinucleotide（NADH） as an indicator of intra-cellular oxygen levels started 50 years *** dysfunction was recognized as a key element in the pathogenesis of various *** developed the "CritiView" —a revolutionary patient monitoring system providing real time data on mitochondrial function as well as microcirculatory blood flow,hemoglobin oxygenation as well as tissue *** hypothesize that under the development of body O2insufficiency the well known blood flow redistribution mechanism will protect the most vital organs（brain and heart） by increasing blood flow while the less vital organs(gastrointestinal（GI） tract or urogenital system) will become hypoperfused and O2delivery will ***,the less vital organs will be the initial responders to O2imbalances and the last to recover after the end of *** urethral wall represents a lessvital organ in the body and may be very sensitive to the development of emergency situations in *** is assumed that the beginning of deterioration processes（i.e.,internal bleeding） as well as resuscitation end-points in critically ill patients will be *** this paper,we review the theoretical,technological,experimental and preliminary clinical results accumulated using the "CritiView".Preliminary clinical studies suggest that our monitoring approach is practical in collecting data from the urethral wall in critical care *** CritiView in critical care medicine may shed new light on body O2balance and the development of body em

关键词： patients monitoring tissue vitality mitochondrial dysfunction tissue blood flow critical care medicine