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https://www.readbyqxmd.com/read/28822845/triphenyl-phosphonium-coated-nano-quercetin-for-oral-delivery-neuroprotective-effects-in-attenuating-age-related-global-moderate-cerebral-ischemia-reperfusion-injury-in-rats
#1
Swarupa Ghosh, Sibani Sarkar, Somsubhra T Choudhury, Tirtha Ghosh, Nirmalendu Das
Cerebral ischemia-reperfusion is a classical example of reactive oxygen species (ROS) mediated acute damage to brain. Post-ischemic reperfusion induced oxygen free radicals production causes damage to brain cell mitochondria. Antioxidants like quercetin (Qc) have potentials to manage oxidative stress related pathophysiology. However low oral bioavailability and poor cell membrane permeability restricts its therapeutic efficacy. To overcome these hurdles mitochondria specific delivery of Qc nanocapsules were designed to efficiently counteract cerebral ischemia-reperfusion induced cell death and neurodegeneration in young and aged rats...
August 16, 2017: Nanomedicine: Nanotechnology, Biology, and Medicine
https://www.readbyqxmd.com/read/28822160/-effects-of-active-components-group-of-xiaoxuming-decoction-on-brain-mitochondria-in-cerebral-ischemia-reperfusion-rats-during-early-recovery-period
#2
Xiao Du, Chang Lu, Xiao-Li He, Guan-Hua Du
To observe the effect of active components group of Xiaoxuming decoction (XXMD) on brain mitochondria in cerebral ischemia/reperfusion rats during early recovery period, and study its protective mechanism for nerves in cerebral ischemia/reperfusion rats during early recovery period. Cerebral ischemia model of middle cerebral artery occlusion in rats was established by suture method, and reperfusion was conducted 2 h later. The degree of cerebral ischemia in rats was evaluated by using Zea-Longa's standard grading method, and the model rats were randomly divided into model group, Xiaoxuming decoction active components low, medium and high dose groups and positive drug Ginaton group, with sham operated rats as control group...
June 2017: Zhongguo Zhong Yao za Zhi, Zhongguo Zhongyao Zazhi, China Journal of Chinese Materia Medica
https://www.readbyqxmd.com/read/28820284/bnip3l-nix-mediated-mitophagy-protects-against-ischemic-brain-injury-independent-of-park2
#3
Yang Yuan, Yanrong Zheng, Xiangnan Zhang, Ying Chen, Xiaoli Wu, Jiaying Wu, Zhe Shen, Lei Jiang, Lu Wang, Wei Yang, Jianhong Luo, Zhenghong Qin, Weiwei Hu, Zhong Chen
Cerebral ischemia induces massive mitochondrial damage. These damaged mitochondria are cleared, thus attenuating brain injury, by mitophagy. Here, we identified the involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy. Bnip3l knockout (bnip3l(-/-)) impaired mitophagy and aggravated cerebral I-R injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in park2(-/-) mice, which showed mitophagy deficiency after I-R...
August 18, 2017: Autophagy
https://www.readbyqxmd.com/read/28817120/the-erythropoietin-derived-peptide-mk-x-and-erythropoietin-have-neuroprotective-effects-against-ischemic-brain-damage
#4
Seung-Jun Yoo, Bongki Cho, Deokho Lee, Gowoon Son, Yeong-Bae Lee, Hyung Soo Han, Eunjoo Kim, Chanil Moon, Cheil Moon
Erythropoietin (EPO) has been well known as a hematopoietic cytokine over the past decades. However, recent reports have demonstrated that EPO plays a neuroprotective role in the central nervous system, and EPO has been considered as a therapeutic target in neurodegenerative diseases such as ischemic stroke. Despite the neuroprotective effect of EPO, clinical trials have shown its unexpected side effects, including undesirable proliferative effects such as erythropoiesis and tumor growth. Therefore, the development of EPO analogs that would confer neuroprotection without adverse effects has been attempted...
August 17, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28811861/importance-of-distinguishing-between-mitochondrial-encephalomyopathy-with-elderly-onset-of-stroke-like-episodes-and-cerebral-infarction
#5
Syuichi Tetsuka, Asako Tagawa, Tomoko Ogawa, Mieko Otsuka, Ritsuo Hashimoto, Hiroyuki Kato
The most common disease-causing mitochondrial DNA (mtDNA) mutation in mitochondrial encephalomyopathy (ME) with lactic acidosis and stroke-like episodes (MELAS) is m.3243A>G. In the future, the incidence of patients with cerebral infarction and diabetes mellitus is expected to increase tremendously. Additionally, the A3243G mutation typical of diabetes is estimated to be present in approximately 2% of all diabetes patients, which suggests that the potential disease population with a mitochondrial disorder is greater than previously thought, and there may have been many cases among the elderly that were misdiagnosed...
September 2017: Journal of Clinical Medicine Research
https://www.readbyqxmd.com/read/28808422/lycium-barbarum-polysaccharides-decrease-hyperglycemia-aggravated-ischemic-brain-injury-through-maintaining-mitochondrial-fission-and-fusion-balance
#6
Wen-Jing Liu, Hai-Feng Jiang, Faisal Ul Rehman, Jing-Wen Zhang, Yue Chang, Li Jing, Jian-Zhong Zhang
Although it has been reported that polysaccharides found in Lycium barbarum possess neuroprotective effects, little is known of their ability to ameliorate hyperglycemia-aggravated ischemia/reperfusion brain injury. In this study, normoglycemic (NG) and hyperglycemic (HG) rats were compared after 30 minutes of middle cerebral artery occlusion (MCAO), followed by 24 or 27 hours of reperfusion, with HG rats pretreated with lyceum barbarum polysaccharides (LBP) or insulin. In each group, the neurological deficit, infarct volume, pathohistology, and expression of proteins, Opa1 and Drp1, were assessed to determine the efficacy of LBP in alleviating hyperglycemia-aggravated ischemia/reperfusion brain injury...
2017: International Journal of Biological Sciences
https://www.readbyqxmd.com/read/28807823/dietary-supplementation-with-acetyl-l-carnitine-counteracts-age-related-alterations-of-mitochondrial-biogenesis-dynamics-and-antioxidant-defenses-in-brain-of-old-rats
#7
Luigi Nicassio, Flavio Fracasso, Giuseppe Sirago, Clara Musicco, Anna Picca, Emanuele Marzetti, Riccardo Calvani, Palmiro Cantatore, Maria Nicola Gadaleta, Vito Pesce
We previously reported the ability of dietary supplementation with acetyl-l-carnitine (ALCAR) to prevent age-related decreases of mitochondrial biogenesis in skeletal muscle and liver of old rats. Here, we investigate the effects of ALCAR supplementation in cerebral hemispheres and cerebellum of old rats by analyzing several parameters linked to mitochondrial biogenesis, mitochondrial dynamics and antioxidant defenses. We measured the level of the coactivators PGC-1α and PGC-1β and of the factors regulating mitochondrial biogenesis, finding an age-related decrease of PGC-1β, whereas PGC-1α level was unvaried...
August 12, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28807772/streptococcus-agalactiae-impairs-cerebral-bioenergetics-in-experimentally-infected-silver-catfish
#8
Matheus D Baldissera, Carine F Souza, Belisa S Parmeggiani, Roberto C V Santos, Guilhian Leipnitz, Karen L S Moreira, Maria Izabel U M da Rocha, Marcelo L da Veiga, Bernardo Baldisserotto
It is becoming evident that bacterial infectious diseases affect brain energy metabolism, where alterations of enzymatic complexes of the mitochondrial respiratory chain and creatine kinase (CK) lead to an impairment of cerebral bioenergetics which contribute to disease pathogenesis in the central nervous system (CNS). Based on this evidence, the aim of this study was to evaluate whether alterations in the activity of complex IV of the respiratory chain and CK contribute to impairment of cerebral bioenergetics during Streptococcus agalactiae infection in silver catfish (Rhamdia quelen)...
August 12, 2017: Microbial Pathogenesis
https://www.readbyqxmd.com/read/28792617/distinctive-cerebral-neuropathology-in-an-adult-case-of-sando-syndrome
#9
Daniel Kirschenbaum, Carola Hedberg-Oldfors, Anders Oldfors, Eduard Scherer, Herbert Budka
The syndrome of sensory ataxic neuropathy with dysarthria and ophthalmoplegia (SANDO), defined genetically by mutations of the gene for the mitochondrial DNA polymerase-γ, POLG, was first described in 1997 (1). Since then, several case reports with various POLG, or more rarely PEO1, mutations have been published (2-4), some specifically addressing muscle and nerve pathology (1, 3), nerve electrophysiology (5), or radiological aspects (4, 6, 7). This article is protected by copyright. All rights reserved.
August 9, 2017: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/28790886/molecular-bases-of-brain-preconditioning
#10
Oleg G Deryagin, Svetlana A Gavrilova, Khalil L Gainutdinov, Anna V Golubeva, Vyatcheslav V Andrianov, Guzel G Yafarova, Sergey V Buravkov, Vladimir B Koshelev
Preconditioning of the brain induces tolerance to the damaging effects of ischemia and prevents cell death in ischemic penumbra. The development of this phenomenon is mediated by mitochondrial adenosine triphosphate-sensitive potassium ([Formula: see text]) channels and nitric oxide signaling (NO). The aim of this study was to investigate the dynamics of molecular changes in mitochondria after ischemic preconditioning (IP) and the effect of pharmacological preconditioning (PhP) with the [Formula: see text]-channels opener diazoxide on NO levels after ischemic stroke in rats...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28777258/knockdown-of-long-noncoding-antisense-rna-brain-derived-neurotrophic-factor-attenuates-hypoxia-reoxygenation-induced-nerve-cell-apoptosis-through-the-bdnf-trkb-pi3k-akt-signaling-pathway
#11
Jian-Bin Zhong, Xie Li, Si-Ming Zhong, Jiu-Di Liu, Chi-Bang Chen, Xiao-Yan Wu
Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal cell apoptosis. The antisense RNA of brain-derived neurotrophic factor (BDNF-AS) is a natural antisense transcript that is transcribed opposite the gene that encodes BDNF. The aim of this study was to determine whether knockdown of BDNF-AS can suppress hypoxia/reoxygenation (H/R)-induced neuronal cell apoptosis and whether this is mediated by the BDNF-TrkB-PI3K/Akt pathway. We detected the expression of BDNF and BDNF-AS in brain tissue from 20 patients with cerebral infarction and five patients with other diseases (but no cerebral ischemia)...
August 2, 2017: Neuroreport
https://www.readbyqxmd.com/read/28768175/neuronal-stimulation-triggers-neuronal-glycolysis-and-not-lactate-uptake
#12
Carlos Manlio Díaz-García, Rebecca Mongeon, Carolina Lahmann, Dorothy Koveal, Hannah Zucker, Gary Yellen
Proper brain function requires a substantial energy supply, up to 20% of whole-body energy in humans, and brain activation produces large dynamic variations in energy demand. While local increases in cerebral blood flow are well known, the cellular responses to energy demand are controversial. During brain excitation, glycolysis of glucose to lactate temporarily exceeds the rate of mitochondrial fuel oxidation; although the increased energy demand occurs mainly within neurons, some have suggested this glycolysis occurs mainly in astrocytes, which then shuttle lactate to neurons as their primary fuel...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28761070/homocysteine-induces-mitochondrial-dysfunction-involving-the-crosstalk-between-oxidative-stress-and-mitochondrial-pstat3-in-rat-ischemic-brain
#13
Shuang Chen, Zhiping Dong, Yaqian Zhao, Na Sai, Xuan Wang, Huan Liu, Guowei Huang, Xumei Zhang
Homocysteine (Hcy) has been shown to have a neurotoxic effect on ischemic brain cells; however, the underlying mechanisms remain incompletely understood. Here, we examined whether Hcy treatment influences mitochondria injury, oxidative stress, and mitochondrial STAT3 (mitoStat3) expression in rat ischemic brain. Our results demonstrated that Hcy treatment aggravated the damage of mitochondrial ultrastructure in the brain cortex and the dentate gyrus region of the hippocampus after focal cerebral ischemia. An elevated Hcy level was also accompanied by the significant inhibition of mitochondrial complex I-III enzymatic activities in addition to an increase in cytochrome c release...
July 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28754131/a-translocator-protein-18%C3%A2-kda-agonist-protects-against-cerebral-ischemia-reperfusion-injury
#14
Han-Dong Li, Minshu Li, Elaine Shi, Wei-Na Jin, Kristofer Wood, Rayna Gonzales, Qiang Liu
BACKGROUND: Cerebral ischemia is a leading cause of death and disability with limited treatment options. Although inflammatory and immune responses participate in ischemic brain injury, the molecular regulators of neuroinflammation after ischemia remain to be defined. Translocator protein 18 kDa (TSPO) mainly localized to the mitochondrial outer membrane is predominantly expressed in glia within the central nervous system during inflammatory conditions. This study investigated the effect of a TSPO agonist, etifoxine, on neuroinflammation and brain injury after ischemia/reperfusion...
July 28, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28752220/a-patient-with-mitochondrial-disorder-due-to-a-novel-mutation-in-mrps22
#15
Mustafa Kılıç, Kader-Karli Oğuz, Esra Kılıç, Deniz Yüksel, Hüseyin Demirci, Mahmut Şamil Sağıroğlu, Didem Yücel-Yılmaz, Rıza Köksal Özgül
MRPS22 gene defect is a very rare newly discovered mitochondrial disorder. We report a 4-month-old severely affected male infant with MRPS22 mutation. Whole exome sequencing revealed a novel homozygous splicing mutation c.339 + 5 G > A in MRPS22 gene. He has mild dysmorphism, hypotonia, developmental delay but not hypertrophic cardiomyopathy and tubulopathy which differ from other majority of reported patients. Therefore, hypertrophic cardiomyopathy and tubulopathy may not be considered as constant features of MRPS22...
July 27, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/28751674/honokiol-suppresses-formyl-peptide-induced-human-neutrophil-activation-by-blocking-formyl-peptide-receptor-1
#16
Fu-Chao Liu, Huang-Ping Yu, Yu-Ting Syu, Jia-You Fang, Chwan-Fwu Lin, Shih-Hsin Chang, Yen-Tung Lee, Tsong-Long Hwang
Formyl peptide receptor 1 (FPR1) mediates bacterial and mitochondrial N-formyl peptides-induced neutrophil activation. Therefore, FPR1 is an important therapeutic target for drugs to treat septic or sterile inflammatory diseases. Honokiol, a major bioactive compound of Magnoliaceae plants, possesses several anti-inflammatory activities. Here, we show that honokiol exhibits an inhibitory effect on FPR1 binding in human neutrophils. Honokiol inhibited superoxide anion generation, reactive oxygen species formation, and elastase release in bacterial or mitochondrial N-formyl peptides (FPR1 agonists)-activated human neutrophils...
July 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28747873/mitochondria-bioenergetics-and-excitotoxicity-new-therapeutic-targets-in-perinatal-brain-injury
#17
REVIEW
Bryan Leaw, Syam Nair, Rebecca Lim, Claire Thornton, Carina Mallard, Henrik Hagberg
Injury to the fragile immature brain is implicated in the manifestation of long-term neurological disorders, including childhood disability such as cerebral palsy, learning disability and behavioral disorders. Advancements in perinatal practice and improved care mean the majority of infants suffering from perinatal brain injury will survive, with many subtle clinical symptoms going undiagnosed until later in life. Hypoxic-ischemia is the dominant cause of perinatal brain injury, and constitutes a significant socioeconomic burden to both developed and developing countries...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28743390/baicalin-attenuates-in-vivo-and-in-vitro-hyperglycemia-exacerbated-ischemia-reperfusion-injury-by-regulating-mitochondrial-function-in-a-manner-dependent-on-ampk
#18
Shanshan Li, Xiaoxu Sun, Lixing Xu, Ruoxi Sun, Zhanqiang Ma, Xueyang Deng, Baolin Liu, Qiang Fu, Rong Qu, Shiping Ma
Cerebral ischemia/reperfusion (I/R) is a lethal and disabling disease. Studies have suggested that hyperglycemia is a risk factor for cerebral I/R. Baicalin is a natural bioactive flavonoid extracted from Scutellaria baicalensis Georgi with neuroprotective activity. In the present study, we investigated the effects of baicalin on hyperglycemia-exacerbated cerebral I/R injury. Streptozotocin (STZ) injection aggravated the brain damage induced by middle cerebral artery occlusion (MCAO) surgery, while baicalin administration reduced blood glucose, relieved neurological deficit and decreased infarct volume...
July 22, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28739363/involvement-of-cerebellum-in-leigh-syndrome-case-report-and-review-of-the-literature
#19
Nitish Chourasia, Rahmat B Adejumo, Rajan P Patel, Mary Kay Koenig
BACKGROUND: Leigh syndrome is an early-onset progressive neurodegenerative disorder typically involving lesions of the bilateral basal ganglia, thalami, and brainstem. Isolated involvement of the cerebellum is uncommon. PATIENT DESCRIPTION: We present a six-year-old boy with Leigh syndrome who presented with recurrent episodes of ataxia and dysarthria. He was diagnosed with Leigh syndrome at two years of age with bilateral basal ganglia lesions on brain magnetic resonance imaging (MRI)...
September 2017: Pediatric Neurology
https://www.readbyqxmd.com/read/28737710/cytoprotective-effect-of-the-ucp2-sirt3-signaling-pathway-by-decreasing-mitochondrial-oxidative-stress-on-cerebral-ischemia-reperfusion-injury
#20
REVIEW
Jing Su, Jie Liu, Xiao-Yu Yan, Yong Zhang, Juan-Juan Zhang, Li-Chao Zhang, Lian-Kun Sun
Recovered blood supply after cerebral ischemia for a certain period of time fails to restore brain function, with more severe dysfunctional problems developing, called cerebral ischemia-reperfusion injury (CIR). CIR involves several extremely complex pathophysiological processes in which the interactions between key factors at various stages have not been fully elucidated. Mitochondrial dysfunction is one of the most important mechanisms of CIR. The mitochondrial deacetylase, sirtuin 3 (SIRT3), can inhibit mitochondrial oxidative stress by deacetylation, to maintain mitochondrial stability...
July 24, 2017: International Journal of Molecular Sciences
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