排序方式: 共有24条查询结果,搜索用时 15 毫秒
1.
de Farias Bianca Xavier Costa Ana Beatriz Engel Nicole Alessandra de Souza Goldim Mariana Pereira da Rosa Turatti Cristini Cargnin-Cavalho Anderson Fortunato Jucélia Jeremias Petronilho Fabricia Jeremias Isabela Casagrande Rezin Gislaine Tezza 《Neurochemical research》2020,45(10):2487-2498
Neurochemical Research - Obesity is characterized by chronic inflammation of low grade. The cholinergic anti-inflammatory pathway favors the reduction of the inflammatory response. In this work the... 相似文献
2.
Piccinini Alexandre Oliveira Mariana Pacheco Silva Mariella Reinol Bett Gabriela Souza Becker Isabel Borges Mendes Talita Farias Salla Daniéle Hendler Silva Larissa Espindola Vilela Thais Ceresér Moraes Fernanda Mendes Moterle Diego Damiani Adriani Paganini Dagostin Lígia Salvan Tietbohl Lariani Tamires Bittencourt João Vitor Silvano Biehl Erica Denicol Tais Luise Bonfante Sandra Regina Andrade Vanessa Moraes Silveira Paulo Cesar Lock Prophiro Josiane Somariva Ferreira Gabriela Kozuchovski Petronilho Fabricia Kanis Luiz Alberto Rezin Gislaine Tezza 《Neurochemical research》2022,47(7):1888-1903
Neurochemical Research - This study aimed to evaluate the effect of Cynara cardunculus leaf ethanol extract on inflammatory and oxidative stress parameters in the hypothalamus, prefrontal cortex,... 相似文献
3.
Ana O. Fagundes Giselli Scaini Patricia M. Santos Monique U. Sachet Nayara M. Bernhardt Gislaine T. Rezin Samira S. Valvassori Patrícia F. Schuck João Quevedo Emilio L. Streck 《Neurochemical research》2010,35(3):405-411
Methylphenidate (MPH) is frequently prescribed for the treatment of attention deficit/hyperactivity disorder. It was previously
demonstrated that MPH altered brain metabolic activity. Most cell energy is obtained through oxidative phosphorylation, in
the mitochondrial respiratory chain. However, there are still few studies about MPH effects on the brain of adult rats. Thus,
in the present study we evaluated the effect of acute or chronic administration of MPH on the activities of mitochondrial
respiratory chain complexes I–IV in the brain of adult rats. For acute administration, a single injection of MPH was given
to 60-day-old rats. For chronic administration, MPH injections were given to 60-day-old rats once daily for 28 days. Our results
showed that complexes I, II, III and IV were inhibited after acute or chronic MPH administration in the hippocampus, prefrontal
cortex, striatum and cerebral cortex. On the other hand, cerebellum was not affected. 相似文献
4.
Ana O. Fagundes Maira R. Aguiar Claudia S. Aguiar Giselli Scaini Monique U. Sachet Nayara M. Bernhardt Gislaine T. Rezin Samira S. Valvassori João Quevedo Emilio L. Streck 《Neurochemical research》2010,35(11):1675-1680
Methylphenidate is commonly used for the treatment of attention deficit/hyperactivity disorder. There are still few works
regarding the effects of methylphenidate on brain energy metabolism. Thus, in the present study we evaluated the effect of
chronic administration of methylphenidate on the activities of mitochondrial respiratory chain complexes I and III in the
brain of young rats. The effect of acute administration of methylphenidate on mitochondrial respiratory chain complexes I,
II, III and IV in the brain of young rats was also investigated. For acute administration, a single injection of methylphenidate
was given to rats on postnatal day 25. For chronic administration, methylphenidate injections were given starting at postnatal
day 25 once daily for 28 days. Our results showed that complexes I and III were not affected by chronic administration of
methylphenidate. Moreover, the acute administration of methylphenidate decreased complex I activity in cerebellum and prefrontal
cortex, whereas complexes II, III and IV were not altered. 相似文献
5.
Búrigo M Roza CA Bassani C Fagundes DA Rezin GT Feier G Dal-Pizzol F Quevedo J Streck EL 《Neurochemical research》2006,31(11):1375-1379
It is well described that impairment of energy production has been implicated in the pathogenesis of a number of diseases. Although several advances have occurred over the past 20 years concerning the use and administration of electroconvulsive therapy (ECT) to minimize its side effects, little progress has been made in understanding its mechanism of action. In this work, our aim was to measure the activities of mitochondrial respiratory chain complexes II and IV and succinate dehydrogenase from rat brain after acute and chronic electroconvulsive shock (ECS). Our results showed that mitochondrial respiratory chain enzymes activities were increased after acute ECS in hippocampus, striatum and cortex of rats. Besides, we also demonstrated that complex II activity was increased after chronic ECS in cortex, while hippocampus and striatum were not affected. Succinate dehydrogenase, however, was inhibited after chronic ECS in striatum, activated in cortex and not affected in hippocampus. Finally, complex IV was not affected by chronic ECS in hippocampus, striatum and cortex. Our findings demonstrated that brain metabolism is altered by ECS. 相似文献
6.
V A Rezin 《Biulleten' eksperimental'no? biologii i meditsiny》1989,108(11):540-542
In the experiments on white rats resuscitated after a 7-minute mechanical asphyxia, phase disorders in the indices of the system of regulation of aggregate state of the blood in postresuscitation period have been revealed. They appear in the shape of a syndrome of disseminated intravascular blood coagulation with the development of hypercoagulation phase by the 3rd hour. Prophylactic introduction of ionol in a dose of 100 mg/kg in 48, 24 and 1 hour before the experiment prevents the development and progressing of the above syndrome. 相似文献
7.
Mitochondrial Dysfunction and Psychiatric Disorders 总被引:1,自引:0,他引:1
Mitochondrial oxidative phosphorylation is the major ATP-producing pathway, which supplies more than 95% of the total energy
requirement in the cells. Damage to the mitochondrial electron transport chain has been suggested to be an important factor
in the pathogenesis of a range of psychiatric disorders. Tissues with high energy demands, such as the brain, contain a large
number of mitochondria, being therefore more susceptible to reduction of the aerobic metabolism. Mitochondrial dysfunction
results from alterations in biochemical cascade and the damage to the mitochondrial electron transport chain has been suggested
to be an important factor in the pathogenesis of a range of neuropsychiatric disorders, such as bipolar disorder, depression
and schizophrenia. Bipolar disorder is a prevalent psychiatric disorder characterized by alternating episodes of mania and
depression. Recent studies have demonstrated that important enzymes involved in brain energy are altered in bipolar disorder
patients and after amphetamine administration, an animal model of mania. Depressive disorders, including major depression,
are serious and disabling. However, the exact pathophysiology of depression is not clearly understood. Several works have
demonstrated that metabolism is impaired in some animal models of depression, induced by chronic stress, especially the activities
of the complexes of mitochondrial respiratory chain. Schizophrenia is a devastating mental disorder characterized by disturbed
thoughts and perception, alongside cognitive and emotional decline associated with a severe reduction in occupational and
social functioning, and in coping abilities. Alterations of mitochondrial oxidative phosphorylation in schizophrenia have
been reported in several brain regions and also in platelets. Abnormal mitochondrial morphology, size and density have all
been reported in the brains of schizophrenic individuals. Considering that several studies link energy impairment to neuronal
death, neurodegeneration and disease, this review article discusses energy impairment as a mechanism underlying the pathophysiology
of some psychiatric disorders, like bipolar disorder, depression and schizophrenia. 相似文献
8.
Tiago P. Freitas Gislaine T. Rezin Cinara L. Gonçalves Gabriela C. Jeremias Lara M. Gomes Giselli Scaini Brena P. Teodorak Samira S. Valvassori João Quevedo Emilio L. Streck 《Molecular and cellular biochemistry》2010,341(1-2):245-249
Bipolar disorder (BD) is a psychiatric disorder characterized by alternating episodes of mania and depression. The intracerebroventricular (i.c.v) administration of ouabain (a Na+/K+-ATPase inhibitor) in rats has been used as an animal model of mania, because present face, construct and predictive validities. Several studies strongly suggest that mitochondrial dysfunction play a central role in the pathophysiology of BD. Citrate synthase (CS) is an enzyme localized in the mitochondrial matrix and represents one of the most important steps of Krebs cycle. The aim of this study was to investigate CS activity in brain of rats after the administration of ouabain. Adult male Wistar rats received a single i.c.v. administration of ouabain (10?2 and 10?3 M) or vehicle (control group). Locomotor activity was measured using the open field task. CS activity was measured in the brain of rats immediately (1 h) and 7 days after ouabain administration. Our results showed that spontaneous locomotion was increased 1 h after ouabain administration, and that the hyperlocomotion persists 7 days after the administration. Moreover, CS activity was inhibited immediately after the administration of ouabain in the prefrontal cortex at the doses of 10?3 and 10?2 M. This inhibition remains by 7 days after the administration of ouabain. On the other hand, it was not observed any difference in CS activity in the hippocampus and striatum. Considering that inhibition of CS activity may reflect a mitochondrial dysfunction, it is tempting to speculate that the reduction of brain energy metabolism might be related to the pathophysiology of BD. 相似文献
9.
Cláudio Sérgio Costa João Vitor Vieira Ronconi Juliana Felipe Daufenbach Cinara Ludvig Gonçalves Gislaine Tezza Rezin Emilio Luiz Streck Marcos Marques da Silva Paula 《Molecular and cellular biochemistry》2010,342(1-2):51-56
Silver has been used for years in medicine; it has known antimicrobial properties. Additionally, silver has been used in water and air filtration to eliminate microorganisms, and, more recently, as a biocide to prevent infections in burns. In contact with the human body, nanoparticles can elicit a spectrum of tissue responses such as the generation of reactive oxygen species, decreased function of mitochondria and even cell death. Mitochondries are intracellular organelles that play a crucial role in ATP production. In the present work, we evaluate the in vitro effect of silver nanoparticles (AgN) on the activities of mitochondrial respiratory chain complexes from the brain, skeletal muscle, heart, and liver of rats. Our results demonstrated that AgN (10, 25, and 50 mg l?1) decreases the activity of mitochondrial respiratory chain complexes I, II, III, and IV from all tissues. 相似文献
10.
Cinara L. Gonçalves Gislaine T. Rezin Gabriela K. Ferreira Isabela C. Jeremias Mariane R. Cardoso Samira S. Valvassori Bruna J. P. Munhoz Gabriela D. Borges Bruno N. Bristot Daniela D. Leffa Vanessa M. Andrade João Quevedo Emilio L. Streck 《Molecular and cellular biochemistry》2013,380(1-2):171-176
Obesity is a chronic and multifactorial disease, whose prevalence is increasing in many countries. Pharmaceutical strategies for the treatment of obesity include drugs that regulate food intake, thermogenesis, fat absorption, and fat metabolism. Fenproporex is the second most commonly consumed amphetamine-based anorectic worldwide; this drug is rapidly converted in vivo into amphetamine, which is associated with neurotoxicity. In this context, the present study evaluated DNA damage parameters in the peripheral blood of young and adult rats submitted to an acute administration and chronic administration of fenproporex. In the acute administration, both young and adult rats received a single injection of fenproporex (6.25, 12.5 or 25 mg/kg i.p.) or vehicle. In the chronic administration, both young and adult rats received one daily injection of fenproporex (6.25, 12.5, or 25 mg/kg i.p.) or Tween for 14 days. 2 h after the last injection, the rats were killed by decapitation and their peripheral blood removed for evaluation of DNA damage parameters by alkaline comet assay. Our study showed that acute administration of fenproporex in young and adult rats presented higher levels of damage index and frequency in the DNA. However, chronic administration of fenproporex in young and adult rats did not alter the levels of DNA damage in both parameters of comet assay. The present findings showed that acute administration of fenproporex promoted damage in DNA, in both young and adult rats. Our results are consistent with other reports which showed that other amphetamine-derived drugs also caused DNA damage. We suggest that the activation of an efficient DNA repair mechanism may occur after chronic exposition to fenproporex. Our results are consistent with other reports that showed some amphetamine-derived drugs also caused DNA damage. 相似文献