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https://www.readbyqxmd.com/read/29456504/a-review-on-central-nervous-system-effects-of-gastrodin
#1
REVIEW
Yuan Liu, Jialiang Gao, Min Peng, Hongyan Meng, Hongbo Ma, Pingping Cai, Yuan Xu, Qiong Zhao, Guomin Si
Rhizoma Gastrodiae (also known as Tian ma ), the dried rhizome of Gastrodia elata Blume, is a famous Chinese herb that has been traditionally used for the treatment of headache, dizziness, spasm, epilepsy, stoke, amnesia and other disorders for centuries. Gastrodin, a phenolic glycoside, is the main bioactive constituent of Rhizoma Gastrodiae . Since identified in 1978, gastrodin has been extensively investigated on its pharmacological properties. In this article, we reviewed the central nervous system (CNS) effects of gastrodin in preclinical models of CNS disorders including epilepsy, Alzheimer's disease, Parkinson's disease, affective disorders, cerebral ischemia/reperfusion, cognitive impairment as well as the underlying mechanisms involved and, where possible, clinical data that support the pharmacological activities...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29454001/brain-bioenergetics-in-rats-with-acute-hyperphenylalaninemia
#2
Nádia Weber Dimer, Bruna Klippel Ferreira, Jotele Fontana Agostini, Maria Luiza Gomes, Luiza Wilges Kist, Fernanda Malgarin, Milena Carvalho-Silva, Lara Mezari Gomes, Joyce Rebelo, Marisa Jádna Silva Frederico, Fátima Regina Mena Barreto Silva, Eduardo Pacheco Rico, Mauricio Reis Bogo, Emilio Luiz Streck, Gustavo Costa Ferreira, Patrícia Fernanda Schuck
Phenylketonuria (PKU) is a disorder of phenylalanine (Phe) metabolism caused by deficient phenylalanine hydroxylase activity. The deficiency results in increased levels of Phe and its metabolites in fluids and tissues of patients. PKU patients present neurological signals and symptoms including hypomyelination and intellectual deficit. This study assessed brain bioenergetics at 1 h after acute Phe administration to induce hyperphenylalaninemia (HPA) in rats. Wistar rats were randomized in two groups: HPA animals received a single subcutaneous administration of Phe (5...
February 14, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29451211/electroacupuncture-preconditioning-protects-against-focal-cerebral-ischemia-reperfusion-injury-via-suppression-of-dynamin-related-protein-1
#3
Gao-Feng Zhang, Pei Yang, Zeng Yin, Huai-Long Chen, Fu-Guo Ma, Bin Wang, Li-Xin Sun, Yan-Lin Bi, Fei Shi, Ming-Shan Wang
Electroacupuncture preconditioning at acupoint Baihui (GV20) can reduce focal cerebral ischemia/reperfusion injury. However, the precise protective mechanism remains unknown. Mitochondrial fission mediated by dynamin-related protein 1 (Drp1) can trigger neuronal apoptosis following cerebral ischemia/reperfusion injury. Herein, we examined the hypothesis that electroacupuncture pretreatment can regulate Drp1, and thus inhibit mitochondrial fission to provide cerebral protection. Rat models of focal cerebral ischemia/reperfusion injury were established by middle cerebral artery occlusion at 24 hours after 5 consecutive days of preconditioning with electroacupuncture at GV20 (depth 2 mm, intensity 1 mA, frequency 2/15 Hz, for 30 minutes, once a day)...
January 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29434700/distinct-magnetic-resonance-imaging-features-in-a-patient-with-novel-rars2-mutations-a-case-report-and-review-of-the-literature
#4
Jie Zhang, Zhongbin Zhang, Yao Zhang, Ye Wu
Pontocerebellar hypoplasia type 6 (PCH6) is a rare autosomal recessive disease that occurs due to mutations in the mitochondrial arginyl-tRNA synthetase 2 (RARS2) gene. To the best of our knowledge, 23 cases with relatively complete clinical data have been reported thus far. In the present study, a case with PCH6 caused by novel RARS2 mutations is described, in which distinct magnetic resonance imaging (MRI) features were identified. In addition, 23 PCH6 cases found in the literature were reviewed. Early onset hypotonia (43...
January 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29433569/mh84-improves-mitochondrial-dysfunction-in-a-mouse-model-of-early-alzheimer-s-disease
#5
Maximilian Pohland, Maren Pellowska, Heike Asseburg, Stephanie Hagl, Martina Reutzel, Aljoscha Joppe, Dirk Berressem, Schamim H Eckert, Mario Wurglics, Manfred Schubert-Zsilavecz, Gunter P Eckert
BACKGROUND: Current approved drugs for Alzheimer's disease (AD) only attenuate symptoms, but do not cure the disease. The pirinixic acid derivate MH84 has been characterized as a dual gamma-secretase/proliferator activated receptor gamma (PPARγ) modulator in vitro. Pharmacokinetic studies in mice showed that MH84 is bioavailable after oral administration and reaches the brain. We recently demonstrated that MH84 improved mitochondrial dysfunction in a cellular model of AD. In the present study, we extended the pharmacological characterization of MH84 to 3-month-old Thy-1 AβPPSL mice (harboring the Swedish and London mutation in human amyloid precursor protein (APP)) which are characterized by enhanced AβPP processing and cerebral mitochondrial dysfunction, representing a mouse model of early AD...
February 13, 2018: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/29431026/the-potential-of-aldehyde-dehydrogenase-2-as-a-therapeutic-target-in-cardiovascular-disease
#6
Thomas Münzel, Andreas Daiber
Mitochondrial aldehyde dehydrogenase (ALDH-2) plays a major role in the ethanol detoxification pathway by removing acetaldehyde. Therefore, ALDH-2 inhibitors such as disulfiram represent the first therapeutic targeting of ALDH-2 for alcoholism therapy. Areas covered: Recently, ALDH-2 was identified as an essential bioactivating enzyme of the anti-ischemic organic nitrate nitroglycerin, bringing ALDH-2 again into the focus of clinical interest. Mechanistic studies on the nitroglycerin bioactivation process revealed that during bioconversion of nitroglycerin and in the presence of reactive oxygen and nitrogen species the active site thiols of ALDH-2 are oxidized and the enzyme activity is lost...
February 10, 2018: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/29427098/mitochondrial-dysfunction-in-huntington-s-disease
#7
Catarina Carmo, Luana Naia, Carla Lopes, A Cristina Rego
Mitochondrial dysfunction has been described as an early pathological mechanism delineating the selective neurodegeneration that occurs in Huntington's disease (HD), a polyglutamine-expansion disorder that largely affects the striatum and the cerebral cortex. Over the years, mitochondria roles in eukaryotic cells (e.g. in neurons) have largely diverged from the classically attributed cell power source; indeed, mitochondria not only contribute for synthesis of several metabolites, but are also dynamic organelles that fragment and fuse to achieve a maximal bioenergetic performance, are transported along microtubules, regulate intracellular calcium homeostasis through the interaction with the endoplasmic reticulum, produce free radicals and participate in cell death processes...
2018: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29424796/activation-of-sigma-1-receptor-by-cutamesine-attenuates-neuronal-apoptosis-by-inhibiting-endoplasmic-reticulum-stress-and-mitochondrial-dysfunction-in-a-rat-model-of-asphyxia-cardiac-arrest
#8
Jiahong Qin, Peng Wang, Yi Li, Lan Yao, Yuanshan Liu, Tao Yu, Jiali Lin, Xiangshao Fang, Zitong Huang
BACKGROUND: Global cerebral ischemic/reperfusion (I/R) injury after cardiac arrest (CA) is a major cause of mortality and morbidity in survivors of resuscitation. We utilized a rat model of asphyxia CA to explore the functional effects and mechanisms of Sigma-1 receptor (Sig-1R) activation in cerebral protection using the Sig-1R agonist cutamesine (SA-4503). METHODS: After resuscitation, the surviving rats were randomly divided into three groups (n = 18 each): (1) the CPR group (0...
February 8, 2018: Shock
https://www.readbyqxmd.com/read/29420160/mito-tempo-prevents-nicotine-induced-exacerbation-of-ischemic-brain-damage
#9
Chun Li, Hong Sun, Guodong Xu, Kimberly D McCarter, Jiyu Li, William G Mayhan
Nicotine may contribute to the pathogenesis of cerebrovascular disease via the generation of reactive oxygen species (ROS). Overproduction of ROS leads to brain damage by intensifying post-ischemic inflammation. Our goal was to determine the effect of Mito-Tempo, a mitochondria-targeted antioxidant, on ischemic brain damage and post-ischemic inflammation during chronic exposure to nicotine. Male Sprague-Dawley rats were divided into four groups: control, nicotine, Mito-Tempo-treated control, and Mito-Tempo-treated nicotine...
February 8, 2018: Journal of Applied Physiology
https://www.readbyqxmd.com/read/29416039/bfgf-plays-a-neuroprotective-role-by-suppressing-excessive-autophagy-and-apoptosis-after-transient-global-cerebral-ischemia-in-rats
#10
Dawei Sun, Wenying Wang, Xintao Wang, Yan Wang, Xiaotao Xu, Feng Ping, Yu Du, Wei Jiang, Derong Cui
Transient global cerebral ischemia (tGCI) is a cerebrovascular disorder that can cause apoptotic neuronal damage and functional deficits. Basic fibroblast growth factor (bFGF) was reported to be highly expressed in the central nervous system (CNS) and to exert neuroprotective effects against different CNS diseases. However, the effects of bFGF on tGCI have not been studied intensively. This study was conducted to investigate the effect of bFGF and its underlying mechanism in an animal model of tGCI. After intracerebroventricular (i...
February 7, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29411248/neuroprotective-effect-and-mechanism-of-action-of-tetramethylpyrazine-nitrone-for-ischemic-stroke-therapy
#11
Gaoxiao Zhang, Tao Zhang, Liangmiao Wu, Xinhua Zhou, Jianbo Gu, Cuimei Li, Wei Liu, Cheng Long, Xifei Yang, Luchen Shan, Lipeng Xu, Yuqiang Wang, Yewei Sun, Zaijun Zhang
Our previous studies demonstrated that the multifunctional agent TBN, a derivative of tetramethylpyrazine armed with a nitrone moiety, displayed high therapeutic efficacy in experimental ischemic stroke models. However, its molecular mechanisms of action underlying the neuroprotective effect need further exploration. In the present study, we found that TBN had significant activities scavenging free radicals such as ·OH, O 2·- and ONOO-, inhibiting Ca2+ overload, maintaining mitochondrial function and preventing neuronal damage in primary cortical cultures...
February 6, 2018: Neuromolecular Medicine
https://www.readbyqxmd.com/read/29410512/clinical-and-molecular-characteristics-of-newly-reported-mitochondrial-disease-entity-caused-by-biallelic-pars2-mutations
#12
Elżbieta Ciara, Dariusz Rokicki, Michal Lazniewski, Hanna Mierzewska, Elżbieta Jurkiewicz, Monika Bekiesińska-Figatowska, Dorota Piekutowska-Abramczuk, Katarzyna Iwanicka-Pronicka, Edyta Szymańska, Piotr Stawiński, Joanna Kosińska, Agnieszka Pollak, Maciej Pronicki, Dariusz Plewczyński, Rafał Płoski, Ewa Pronicka
Most of the 19 mitochondrial aminoacyl-tRNA synthetases (mt-aaRSs) involved in mitochondrial protein synthesis are already linked to specific entities, one of the exceptions being PARS2 mutations for which pathogenic significance is not finally validated. The aim of the study was to characterize the PARS2- related phenotype.Three siblings with biallelic PARS2 mutations presented from birth with infantile spasms, secondary microcephaly, and similar facial dysmorphy. Mental development was deeply impaired with speech absence and no eye contact...
February 6, 2018: Journal of Human Genetics
https://www.readbyqxmd.com/read/29408517/clinical-features-of-lonp1-related-infantile-cataract
#13
Arif O Khan, Amani AlBakri
Biallelic mutations in the nuclear gene LONP1 (LON peptidase 1, mitochondrial) cause CODAS syndrome (cerebral, ocular, dental, auricular, and skeletal anomalies), a systemic disease that can include infantile cataract. However, we have found that biallelic mutations in the gene can also underlie infantile cataract in the setting of minimal or no apparent extraocular findings. This report highlights our clinical experience with children referred for the management of infantile cataract who were found to harbor biallelic LONP1 gene mutations...
February 3, 2018: Journal of AAPOS: the Official Publication of the American Association for Pediatric Ophthalmology and Strabismus
https://www.readbyqxmd.com/read/29405550/treatment-with-the-mitochondrial-targeted-antioxidant-peptide-ss-31-rescues-neurovascular-coupling-responses-and-cerebrovascular-endothelial-function-and-improves-cognition-in-aged-mice
#14
Stefano Tarantini, Noa M Valcarcel-Ares, Andriy Yabluchanskiy, Gabor A Fulop, Peter Hertelendy, Tripti Gautam, Eszter Farkas, Aleksandra Perz, Peter S Rabinovitch, William E Sonntag, Anna Csiszar, Zoltan Ungvari
Moment-to-moment adjustment of cerebral blood flow (CBF) via neurovascular coupling has an essential role in maintenance of healthy cognitive function. In advanced age, increased oxidative stress and cerebromicrovascular endothelial dysfunction impair neurovascular coupling, likely contributing to age-related decline of higher cortical functions. There is increasing evidence showing that mitochondrial oxidative stress plays a critical role in a range of age-related cellular impairments, but its role in neurovascular uncoupling remains unexplored...
February 6, 2018: Aging Cell
https://www.readbyqxmd.com/read/29397560/buttermilk-and-krill-oil-phospholipids-improve-hippocampal-insulin-resistance-and-synaptic-signaling-in-aged-rats
#15
Joao Tomé-Carneiro, M Carmen Crespo, Emma Burgos-Ramos, Cristina Tomas-Zapico, Alba García-Serrano, Pilar Castro-Gómez, Cesar Venero, Inmaculada Pereda-Pérez, Shishir Baliyan, Azucena Valencia, Javier Fontecha, Alberto Dávalos, Francesco Visioli
Impaired glucose metabolism and mitochondrial decay greatly increase with age, when cognitive decline becomes rampant. No pharmacological or dietary intervention has proven effective, but proper diet and lifestyle do postpone the onset of neurodegeneration and some nutrients are being investigated. We studied insulin signaling, mitochondrial activity and biogenesis, and synaptic signaling in the hippocampus and cortex following dietary supplementation with bioactive phospholipid concentrates of krill oil (KOC), buttermilk fat globule membranes (BMFC), and a combination of both in aged rats...
February 3, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29393465/puerarin-inhibits-non-small-cell-lung-cancer-cell-growth-via-the-induction-of-apoptosis
#16
Yefang Hu, Xi Li, Ling Lin, Siting Liang, Jian Yan
Puerarin, an isoflavone isolated from Kudzu roots, has been demonstrated to have beneficial effect on cardiovascular and cerebral vascular diseases. Recently research has revealed that puerarin exerts an anticancer role in many different types of cancer. The aim of the present study was to investigate the antitumor effects of puerarin on non-small cell lung cancer (NSCLC). Treatment of puerarin significantly inhibited the growth of NSCLC cell lines as determined by CCK-8 kit in vitro. Flow cytometry results indicated that puerarin treatments promoted NSCLC cell apoptosis...
January 26, 2018: Oncology Reports
https://www.readbyqxmd.com/read/29391077/cerebral-manifestations-of-mitochondrial-disorders
#17
Josef Finsterer, Elmano Henrique Torres de Carvalho
This review aims at summarizing and discussing previous and recent findings concerning the cerebral manifestations of mitochondrial disorders (MIDs). MIDs frequently present as mitochondrial multiorgan disorder syndrome (MIMODS) either already at onset or later in the course. After the muscle, the brain is the organ second most frequently affected in MIMODS. Cerebral manifestations of MIDs are variable and may present with or without a lesion on imaging or functional studies, but there can be imaging/functional lesions without clinical manifestations...
November 2017: Canadian Journal of Neurological Sciences. le Journal Canadien des Sciences Neurologiques
https://www.readbyqxmd.com/read/29387001/rosuvastatin-improves-neurite-outgrowth-of-cortical-neurons-against-oxygen-glucose-deprivation-via-notch1-mediated-mitochondrial-biogenesis-and-functional-improvement
#18
Weiliang He, Yingping Liu, Xiaochao Tian
Neurogenesis, especially neurite outgrowth is an essential element of neuroplasticity after cerebral ischemic injury. Mitochondria may supply ATP to power fundamental developmental processes including neuroplasticity. Although rosuvastatin (RSV) displays a potential protective effect against cerebral ischemia, it remains unknown whether it modulates mitochondrial biogenesis and function during neurite outgrowth. Here, the oxygen-glucose deprivation (OGD) model was used to induce ischemic injury. We demonstrate that RSV treatment significantly increases neurite outgrowth in cortical neurons after OGD-induced damage...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29380912/ubiquinol-treatment-for-tbi-in-male-rats-effects-on-mitochondrial-integrity-injury-severity-and-neurometabolism
#19
Janet D Pierce, Raeesa Gupte, Amanda Thimmesch, Qiuhua Shen, John B Hiebert, William M Brooks, Richard L Clancy, Francisco J Diaz, Janna L Harris
Following traumatic brain injury (TBI), there is significant secondary damage to cerebral tissue from increased free radicals and impaired mitochondrial function. This imbalance between reactive oxygen species (ROS) production and the effectiveness of cellular antioxidant defenses is termed oxidative stress. Often there are insufficient antioxidants to scavenge ROS, leading to alterations in cerebral structure and function. Attenuating oxidative stress following a TBI by administering an antioxidant may decrease secondary brain injury, and currently many drugs and supplements are being investigated...
January 30, 2018: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29379271/sinomenine-reduces-neuronal-cell-apoptosis-in-mice-after-traumatic-brain-injury-via-its-effect-on-mitochondrial-pathway
#20
Chuanjing Fu, Qi Wang, Xiaofu Zhai, Juemin Gao
Background: Sinomenine (SIN) has been shown to have protective effects against brain damage following traumatic brain injury (TBI). However, the mechanisms and its role in these effects remain unclear. This study was conducted to investigate the potential mechanisms of the protective effects of SIN. Methods: The weight-drop model of TBI in Institute of Cancer Research (ICR) mice were treated with SIN or a vehicle via intraperitoneal administration 30 min after TBI...
2018: Drug Design, Development and Therapy
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