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https://www.readbyqxmd.com/read/28443065/hemoglobin-improved-protection-in-cultured-cerebral-cortical-astroglial-cells-inhibition-of-oxidative-stress-and-caspase-activation
#1
Fatma Amri, Ikram Ghouili, Marie-Christine Tonon, Mohamed Amri, Olfa Masmoudi-Kouki
Oxidative stress plays a major role in triggering astroglial cell death in diverse neuropathological conditions such as ischemia and neurodegenerative diseases. Numerous studies indicate that hemoglobin (Hb) is expressed in both resting and reactive glia cells, but nothing is known regarding a possible role of Hb on astroglial cell survival. Thus, the purpose of the present study was to investigate the potential glioprotective effect of Hb on hydrogen peroxide (H2O2)-induced oxidative stress and apoptosis in cultured rat astrocytes...
2017: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/28440425/mitochondrial-transcription-factor-a-tfam-is-upregulated-in-glioma
#2
Hyunji Lee, Jisoo Park, Quangdon Tran, Dohoon Kim, Youngeun Hong, Hyeonjeong Cho, So Hee Kwon, Derek Brazil, Seon-Hwan Kim, Jongsun Park
Mitochondrial transcription factor A (TFAM), which was initially discovered as a transcription factor for mitochondrial DNA, has known to be critical for the regulation of mitochondrial DNA. However the possible involvement of TFAM in cancer is largely unknown. In this study, we have provided some evidence that TFAM may have a potential role in brain tumor. Western blot analysis with anti‑TFAM antibody indicated that TFAM is overexpressed in glioblastoma cell lines including U87MG and U251MG. Transcriptome profiling of U87MG and U251MG cells by using deep‑sequencing revealed that TFAM transcripts were upregulated in these cells compared to its of cerebral cortex...
April 12, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28438718/the-effect-of-50-compared-to-100-inspired-oxygen-fraction-on-brain-oxygenation-and-post-cardiac-arrest-mitochondrial-function-in-experimental-cardiac-arrest
#3
Annika Nelskyla, Jouni Nurmi, Milla Jousi, Alexey Schramko, Eero Mervaala, Giuseppe Ristagno, Markus B Skrifvars
BACKGROUND AND AIM: We hypothesised that the use of 50% compared to 100% oxygen maintains cerebral oxygenation and ameliorates the disturbance of cardiac mitochondrial respiration during cardiopulmonary resuscitation (CPR). METHODS: Ventricular fibrillation (VF) was induced electrically in anaesthetised healthy adult pigs and left untreated for seven minutes followed by randomisation to manual ventilation with 50% or 100% oxygen and mechanical chest compressions (LUCAS(®))...
April 21, 2017: Resuscitation
https://www.readbyqxmd.com/read/28436815/moyamoya-in-a-patient-with-fires-a-first-case-report
#4
Taylor Kaufman, Andrew White
Febrile infection-related epilepsy syndrome (FIRES) is a form of epileptic encephalopathy with severe refractory epilepsy that presents in previously healthy, school-aged children after significant febrile illness with concomitant rise in body temperature. Suspected causes include genetic or acquired channelopathies, as well as mitochondrial disturbances. In FIRES, the EEG shows diffuse slowing, generalized, and/or multifocal discharges. Seizures are present and resistant to treatment. Moyamoya angiopathy (MMA) is characterized by progressive stenosis of cerebral arteries and subsequent development of a network of collateral circulation that is prone to rupture...
2017: Neurodiagnostic Journal
https://www.readbyqxmd.com/read/28431972/mitochondrial-energy-metabolism-of-rat-hippocampus-after-treatment-with-the-antidepressants-desipramine-and-fluoxetine
#5
Roberto Federico Villa, Federica Ferrari, Laura Bagini, Antonella Gorini, Nicoletta Brunello, Fabio Tascedda
Alterations in mitochondrial functions have been hypothesized to participate in the pathogenesis of depression, because brain bioenergetic abnormalities have been detected in depressed patients by neuroimaging in vivo studies. However, this hypothesis is not clearly demonstrated in experimental studies: some suggest that antidepressants are inhibitors of mitochondrial metabolism, while others observe the opposite. In this study, the effects of 21-day treatment with desipramine (15 mg/kg) and fluoxetine (10 mg/kg) were examined on the energy metabolism of rat hippocampus, evaluating the catalytic activity of regulatory enzymes of mitochondrial energy-yielding metabolic pathways...
April 18, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28429368/-aralar-agc1-deficiency-a-neurodevelopmental-disorder-with-severe-impairment-of-neuronal-mitochondrial-respiration-does-not-produce-a-primary-increase-in-brain-lactate
#6
Inés Juaristi, María L García-Martin, Tiago B Rodrigues, Jorgina Satrústegui, Irene Llorente-Folch, Beatriz Pardo
ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS). AGC1-deficiency is a rare disease causing global cerebral hypomyelination, developmental arrest, hypotonia, and epilepsy (OMIM ID #612949); the aralar-KO mouse recapitulates the major findings in humans. This study was aimed at understanding the impact of ARALAR-deficiency in brain lactate levels as a biomarker. We report that lactate was equally abundant in wild-type and aralar-KO mouse brain in vivo at PND 17...
April 21, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28428752/desensitizing-mitochondrial-permeability-transition-by-erk-cyclophilin-d-axis-contributes-to-the-neuroprotective-effect-of-gallic-acid-against-cerebral-ischemia-reperfusion-injury
#7
Jing Sun, Da-Dui Ren, Jin-Yi Wan, Chen Chen, Dong Chen, Huan Yang, Chun-Lai Feng, Jing Gao
Ischemic stroke is a devastating disease with complex pathophysiology. Much evidence confirms that opening of the mitochondrial permeability transition pore (MPTP) is related with mitochondrial dysfunction to apoptosis in ischemic stroke, thus elucidating its signaling mechanism and screening novel MPTP inhibitor is therefore of paramount importance. Our earlier studies identified that gallic acid (GA), a naturally occurring plant phenol, endows with effect on inhibition of mitochondrial dysfunction, which has significant neuroprotective effect in cerebral ischemia/reperfusion injury...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28427446/respiratory-chain-complex-iii-deficiency-due-to-mutated-bcs1l-a-novel-phenotype-with-encephalomyopathy-partially-phenocopied-in-a-bcs1l-mutant-mouse-model
#8
Saara Tegelberg, Nikica Tomašić, Jukka Kallijärvi, Janne Purhonen, Eskil Elmér, Eva Lindberg, David Gisselsson Nord, Maria Soller, Nicole Lesko, Anna Wedell, Helene Bruhn, Christoph Freyer, Henrik Stranneheim, Rolf Wibom, Inger Nennesmo, Anna Wredenberg, Erik A Eklund, Vineta Fellman
BACKGROUND: Mitochondrial diseases due to defective respiratory chain complex III (CIII) are relatively uncommon. The assembly of the eleven-subunit CIII is completed by the insertion of the Rieske iron-sulfur protein, a process for which BCS1L protein is indispensable. Mutations in the BCS1L gene constitute the most common diagnosed cause of CIII deficiency, and the phenotypic spectrum arising from mutations in this gene is wide. RESULTS: A case of CIII deficiency was investigated in depth to assess respiratory chain function and assembly, and brain, skeletal muscle and liver histology...
April 20, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28413987/alzheimer-s-disease-like-early-phase-brain-pathogenesis-self-curing-amelioration-of-neurodegeneration-from-pro-inflammatory-wounding-to-anti-inflammatory-healing
#9
Jiang He, Tao Liao, Guo-Xin Zhong, Ji-Da Zhang, Yan-Ping Chen, Qi Wang, Qing-Ping Zeng
The etiological initiators of neuroinflammation remain inclusive, and effective interventions to block neurodegeneration are unavailable. Surprisingly, we found collagen II-combined complete Freund's adjuvant (CC) that usually induces rheumatoid arthritis (RA) also drives Alzheimer's disease (AD)-like neurodegeneration in mice. CC not only upregulates the cerebral pro-inflammatory cytokines including tumor necrosis factor α (TNF-α) and interleukin 8 (IL-8), but also downregulates the cerebral interleukin 10 (IL-10), an anti-inflammatory cytokine, and tyrosine hydroxylase (TH), a rate-limiting enzyme for biosynthesis of the anti-inflammatory neurotransmitter dopamine...
April 17, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28401402/ischemia-reperfusion-induced-translocation-of-pkc%C3%AE-ii-to-mitochondria-as-an-important-mediator-of-a-protective-signaling-mechanism-in-an-ischemia-resistant-region-of-the-hippocampus
#10
Olga Krupska, Anna Sarnowska, Bartlomiej Fedorczyk, Magdalena Gewartowska, Aleksandra Misicka, Barbara Zablocka, Malgorzata Beresewicz
Emerging reports indicate that activated PKC isoforms that translocate to the mitochondria are pro- or anti-apoptotic to mitochondrial function. Here, we concentrate on the role of PKCβ translocated to mitochondria in relation to the fate of neurons following cerebral ischemia. As we have demonstrated previously ischemia/reperfusion injury (I/R) results in translocation of PKCβ from cytoplasm to mitochondria, but only in ischemia-resistant regions of the hippocampus (CA2-4, DG), we hypothesize that this translocation may be a mediator of a protective signaling mechanism in this region...
April 12, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28400805/3-daidzein-sulfonate-sodium-improves-mitochondrial-functions-after-cerebral-ischemia-reperfusion-injury
#11
Wa Yuan, Qin Chen, Jing Zeng, Hai Xiao, Zhi-Hua Huang, Xiao Li, Qiong Lei
3'-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein (an active ingredient of the kudzu vine root). It has been shown to have a protective effect on cerebral ischemia/reperfusion injury in rats. We plan to study the mechanism of its protective effect. 3'-Daidzein sulfonate sodium was injected in rats after cerebral ischemia/reperfusion injury. Results showed that 3'-daidzein sulfonate sodium significantly reduced mitochondrial swelling, significantly elevated the mitochondrial membrane potential, increased mitochondrial superoxide dismutase and glutathione peroxidase activities, and decreased mitochondrial malondialdehyde levels...
February 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28396174/sirt3-confers-protection-against-neuronal-ischemia-by-inducing-autophagy-involvement-of-the-ampk-mtor-pathway
#12
Shu-Hui Dai, Tao Chen, Xia Li, Kang-Yi Yue, Peng Luo, Li-Kun Yang, Jie Zhu, Yu-Hai Wang, Zhou Fei, Xiao-Fan Jiang
Sirtuin3 (Sirt3) is a member of the silent information regulator 2 (Sir2) family of proteins located in mitochondria that influences almost every major aspect of mitochondrial biology, including ATP generation and reactive oxygen species (ROS) production. Our previous study showed that Sirt3 exerts protective effects against oxidative stress in neuronal cells. In this study, we investigated the role of Sirt3 in neuronal ischemia using an oxygen and glucose deprivation (OGD) model. Sirt3 was up-regulated by OGD and overexpression of Sirt3 through lentivirus transfection significantly reduced OGD-induced lactate dehydrogenase (LDH) release and neuronal apoptosis...
April 7, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28392696/compound-porcine-cerebroside-and-ganglioside-injection-attenuates-cerebral-ischemia-reperfusion-injury-in-rats-by-targeting-multiple-cellular-processes
#13
Mingyang Wang, Yi Zhang, Lu Feng, Ji Zheng, Shujie Fan, Junya Liu, Nan Yang, Yanyong Liu, Pingping Zuo
BACKGROUND: Compound porcine cerebroside and ganglioside injection (CPCGI) is a neurotrophic drug used clinically to treat certain functional disorders of brain. Despite its extensive usage throughout China, the exact mechanistic targets of CPCGI are unknown. This study was carried out to investigate the protective effect of CPCGI against ischemic neuronal damage in rats with middle cerebral artery occlusion (MCAO) reperfusion injury and to investigate the neuroprotective mechanisms of CPCGI...
2017: Neuropsychiatric Disease and Treatment
https://www.readbyqxmd.com/read/28386847/inhibition-of-intracellular-type-10-adenylyl-cyclase-protects-cortical-neurons-against-reperfusion-induced-mitochondrial-injury-and-apoptosis
#14
Megha Chagtoo, Nelson George, Neelam Pathak, Swasti Tiwari, Madan M Godbole, Yury Ladilov
Mitochondrial injury significantly contributes to the neuronal death under cerebral ischemia and reperfusion. Within several signaling pathways, cyclic adenosine monophosphate (cAMP) signaling plays a substantial role in mitochondrial injury and cell death. Traditionally, the source of cellular cAMP has been attributed to the membrane-bound adenylyl cyclase, whereas the role of the intracellular localized type 10 soluble adenylyl cyclase (sAC) in neuronal pathology has not been considered. Since neurons express an active form of sAC, we aimed to investigate the role of sAC in reperfusion-induced neuronal apoptosis...
April 6, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28372990/neurotoxic-mechanisms-by-which-the-usp14-inhibitor-iu1-depletes-ubiquitinated-proteins-and-tau-in-rat-cerebral-cortical-neurons-relevance-to-alzheimer-s-disease
#15
Magdalena J Kiprowska, Anna Stepanova, Dustin R Todaro, Alexander Galkin, Arthur Haas, Scott M Wilson, Maria E Figueiredo-Pereira
In Alzheimer's disease proteasome activity is reportedly downregulated, thus increasing it could be therapeutically beneficial. The proteasome-associated deubiquitinase USP14 disassembles polyubiquitin-chains, potentially delaying proteasome-dependent protein degradation. We assessed the protective efficacy of inhibiting or downregulating USP14 in rat and mouse (Usp14(axJ)) neuronal cultures treated with prostaglandin J2 (PGJ2). IU1 concentrations (HIU1>25μM) reported by others to inhibit USP14 and be protective in non-neuronal cells, reduced PGJ2-induced Ub-protein accumulation in neurons...
March 31, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28363987/progesterone-induced-neuroprotection-in-reperfusion-promoted-mitochondrial-dysfunction-following-focal-cerebral-ischemia-in-rats
#16
Syed Suhail Andrabi, Suhel Parvez, Heena Tabassum
Alterations in mitochondrial permeability transition and organelle damage are key players in the development of cerebral ischemic tissue injury due to associated modifications in ATP turnover and cellular apoptosis/necrosis. Early restoration of blood flow and improvement of mitochondrial function might reverse the situation and help in recovery following an onset of stroke. Mitochondria and related bioenergetics can be effectively used as pharmacological targets. Progesterone (P4), one of the promising neurosteroids, has been found neuroprotective in various models of neurological diseases through a number of mechanisms...
March 31, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28332767/bcap31-associated-encephalopathy-and-complex-movement-disorder-mimicking-mitochondrial-encephalopathy
#17
Saleh Albanyan, Amal Al Teneiji, Nasim Monfared, Saadet Mercimek-Mahmutoglu
BCAP31, encoded by BCAP31, is involved in the export of transmembrane proteins from the endoplasmic reticulum. Pathogenic variants in BCAP31 results in global developmental delay, dystonia, deafness and dysmorphic features in males, called deafness, dystonia, and cerebral hypomyelination (DDCH) syndrome. We report a new patient with BCAP3-associated encephalopathy, DDCH syndrome, sensorineural hearing loss, generalized dystonia, and choreoathetosis. This 3.5-year-old boy had microcephaly and failure to thrive within the first 3 months of life...
March 23, 2017: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/28322157/diabetes-related-neurological-implications-and-pharmacogenomics
#18
Rojas Carranza Camilo Andrés, Bustos Cruz Rosa Helena, Pino Pinzón Carmen Juliana, Ariza Marquez Yeimy Viviana, Gómez Bello Rosa Margarita, Cañadas Garre Marisa
Diabetes mellitus (DM) is the most commonly occurring cause of neuropathy around the world and is beginning to grow in countries where there is a risk of obesity. DM Type II, (T2DM) is a common age-related disease and is a major health concern, particularly in developed countries in Europe where the population is aging. T2DM is a chronic disease which is characterised by hyperglycemia, hyperinsulinemia and insulin resistance, together with the body's inability to use glucose as energy. Such metabolic disorder produces a chronic inflammatory state, as well as changes in lipid metabolism leading to hypertriglyceridemia, thereby producing chronic deterioration of the organs and premature morbidity and mortality...
March 17, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28320189/tempol-4-hydroxy-tempo-inhibits-anoxia-induced-progression-of-mitochondrial-dysfunction-and-associated-neurobehavioral-impairment-in-neonatal-rats
#19
Puneet K Samaiya, Gopeshwar Narayan, Ashok Kumar, Sairam Krishnamurthy
BACKGROUND: Anoxia leads to a robust generation of reactive oxygen species/nitrogen species which can result in mitochondrial dysfunction and associated cell death in the cerebral cortex of neonates. AIM: The present study investigated the pharmacological role of tempol in the treatment of rat neonatal cortical mitochondrial dysfunction induced insult progression (day-1 to day-7) and associated neurobehavioral alterations post-anoxia. METHODS: Rat pups of 30h age or postnatal day 2 (PND2) were randomly divided into 5 groups (n=5 per group): (1) Control; (2) Anoxia; (3) Anoxia+Tempol 75mg/kg; (4) Anoxia+Tempol 150mg/kg; and (5) Anoxia+Tempol 300mg/kg, and subjected to two episode of anoxia (10min each) at 24h of time interval in an enclosed chamber supplied with 100% N2...
April 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28320180/mitochondrial-dysfunction-silent-killer-in-cerebral-ischemia
#20
REVIEW
Pramila Bakthavachalam, Prakash Srinivasan Timiri Shanmugam
Mitochondrial dysfunction aggravates ischemic neuronal injury through activation of various pathophysiological and molecular mechanisms. Ischemic neuronal injury is particularly intensified during reperfusion due to impairment of mitochondrial function. Mitochondrial mutilation instigates alterations in calcium homeostasis in neurons, which plays a pivotal role in the maintenance of normal neuronal function. Increase in intracellular calcium level in mitochondria triggers the opening of mitochondrial transition pore and over production of reactive oxygen species (ROS)...
April 15, 2017: Journal of the Neurological Sciences
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