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1.
Neuromolecular Med ; 26(1): 4, 2024 Mar 08.
Artigo em Inglês | MEDLINE | ID: mdl-38457013

RESUMO

BACKGROUND: Ischemic stroke is the leading cause of mortality and disability worldwide with more than half of survivors living with serious neurological sequelae; thus, it has recently attracted a lot of attention in the field of medical study. PURPOSE: The aim of this study was to determine the effect of naringin supplementation on neurogenesis and brain-derived neurotrophic factor (BDNF) levels in the brain in experimental brain ischemia-reperfusion. STUDY DESIGN: The research was carried out on 40 male Wistar-type rats (10-12 weeks old) obtained from the Experimental Animals Research and Application Center of Selçuk University. Experimental groups were as follows: (1) Control group, (2) Sham group, (3) Brain ischemia-reperfusion group, (4) Brain ischemia-reperfusion + vehicle group (administered for 14 days), and (5) Brain ischemia-reperfusion + Naringin group (100 mg/kg/day administered for 14 days). METHODS: In the ischemia-reperfusion groups, global ischemia was performed in the brain by ligation of the right and left carotid arteries for 30 min. Naringin was administered to experimental animals by intragastric route for 14 days following reperfusion. The training phase of the rotarod test was started 4 days before ischemia-reperfusion, and the test phase together with neurological scoring was performed the day before and 1, 7, and 14 days after the operation. At the end of the experiment, animals were sacrificed, and then hippocampus and frontal cortex tissues were taken from the brain. Double cortin marker (DCX), neuronal nuclear antigen marker (NeuN), and BDNF were evaluated in hippocampus and frontal cortex tissues by Real-Time qPCR analysis and immunohistochemistry methods. RESULTS: While ischemia-reperfusion increased the neurological score values, DCX, NeuN, and BDNF levels decreased significantly after ischemia in the hippocampus and frontal cortex tissues. However, naringin supplementation restored the deterioration to a certain extent. CONCLUSION: The results of the study show that 2 weeks of naringin supplementation may have protective effects on impaired neurogenesis and BDNF levels after brain ischemia and reperfusion in rats.


Assuntos
Isquemia Encefálica , Fator Neurotrófico Derivado do Encéfalo , Flavanonas , Humanos , Ratos , Masculino , Animais , Fator Neurotrófico Derivado do Encéfalo/genética , Ratos Wistar , Isquemia Encefálica/tratamento farmacológico , Reperfusão , Neurogênese , Isquemia , Suplementos Nutricionais
2.
Artif Organs ; 41(8): 744-752, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28261890

RESUMO

The cochlea is an end organ, which is metabolically dependent on a nutrient and oxygen supply to maintain its normal physiological function. Cochlear ischemia and reperfusion (IR) injury is considered one of the most important causes of human idiopathic sudden sensorineural hearing loss. The aim of the present study was to study the efficacy of ozone therapy against cochlear damage caused by IR injury and to investigate the potential clinical use of this treatment for sudden deafness. Twenty-eight guinea pigs were randomized into four groups. The sham group (S) (n = 7) was administered physiological saline intraperitoneally (i.p.) for 7 days. The ozone group (O) (n = 7) was administered 1 mg/kg of ozone i.p. for 7 days. In the IR + O group (n = 7), 1 mg/kg of ozone was administered i.p. for 7 days before IR injury. On the eighth day, the IR + O group was subjected to cochlear ischemia for 15 min by occluding the bilateral vertebral artery and vein with a nontraumatic clamp and then reperfusion for 2 h. The IR group was subjected to cochlear IR injury. After the IR procedure, the guinea pigs were sacrificed on the same day. In a general histological evaluation, cochlear and spiral ganglionic tissues were examined with a light microscope, and apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The apoptotic index (AI) was then calculated. Blood samples were sent for analyses of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase, malondialdehyde (MDA), the total oxidant score (TOS), and total antioxidant capacity (TAC). Data were evaluated statistically using the Kruskal-Wallis test. The AI was highest in the IR group. The AI of the IR + O group was lower than that of the IR group. The biochemical antioxidant parameters SOD and GSH-Px and the TAC values were highest in the O group and lowest in the IR group. The MDA level and TOS were highest in the IR group and lowest in the O group. Controlled ozone administration stimulated endogenous antioxidant defense systems, thereby helping the body to combat IR injury. Although this study revealed a statistically significant decrease in cochlear IR damage following ozone therapy, further studies will be necessary to explain the protective mechanisms of ozone therapy in cochlear IR injury.


Assuntos
Cóclea/efeitos dos fármacos , Cóclea/patologia , Doenças Cocleares/etiologia , Doenças Cocleares/prevenção & controle , Ozônio/uso terapêutico , Substâncias Protetoras/uso terapêutico , Traumatismo por Reperfusão/complicações , Animais , Apoptose/efeitos dos fármacos , Cóclea/metabolismo , Doenças Cocleares/metabolismo , Doenças Cocleares/patologia , Cobaias , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ozônio/administração & dosagem , Substâncias Protetoras/administração & dosagem
3.
J Membr Biol ; 246(1): 1-6, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22915054

RESUMO

More than 600 chemicals can cause damage in liver, one of which is carbon tetrachloride (CCl4). Hepatoprotective agents could prevent tissue damage and reduce morbidity and mortality rates; such agents may include alternative or folkloric treatments. We investigated sesame (Sesamum indicum L.) for its hepatoprotective effect in CCl4-induced experimental liver damage. To this end, 0.8 mg/kg of sesame fixed oil was provided intraperitoneally to rats whose livers were damaged by CCl4. Tissue and blood samples were taken at the end of the experiments and evaluated histologically and biochemically. Ballooning degenerations and an increase in lipid droplets in liver parenchyma and increases in serum alanine transaminase, aspartate transaminase, and bilirubin were found in the CCl4 group. Biochemical and histopathological findings in the sesame fixed oil treated group were not significantly different from the CCl4 group. Sesame did not show a hepatoprotective effect in CCl4-induced liver toxicity.


Assuntos
Tetracloreto de Carbono/toxicidade , Fígado/efeitos dos fármacos , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêutico , Sesamum/química , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Doença Hepática Induzida por Substâncias e Drogas/sangue , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Fígado/patologia , Masculino , Ratos , Ratos Sprague-Dawley
4.
Phytother Res ; 20(6): 500-3, 2006 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-16619345

RESUMO

The present study investigated the analgesic and hepatoprotective activities of a water extract of Ononis spinosa L. (OS) in mice. Analgesic activity was based on the pain thresholds measured with the tail-flick test before administration at 30, 90 and 150 min. The results were analysed with one-way variance analysis. The extract of Ononis spinosa showed analgesic activity equivalent to aspirin at 30 and 90 min and even higher than aspirin with the 50 mg/kg dose. At a dose of 100 mg/kg OS showed an analgesic effect equivalent to aspirin at all time points.The hepatoprotective influence of OS on carbon tetrachloride (CCl(4))-induced acute liver toxicity was also studied. The extract had no significant effect on the increased levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and bilirubin in CCl(4) treated animals (p > 0.05). Thus, the results reveal that the extract of OS had no hepatoprotective effect on CCl(4)-induced acute liver toxicity.


Assuntos
Analgésicos/análise , Fabaceae/química , Fígado/efeitos dos fármacos , Nociceptores/efeitos dos fármacos , Extratos Vegetais/farmacologia , Alanina Transaminase/efeitos dos fármacos , Animais , Aspartato Aminotransferases/efeitos dos fármacos , Bilirrubina/metabolismo , Peso Corporal/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Masculino , Camundongos , Ratos , Ratos Sprague-Dawley
5.
Toxicol Appl Pharmacol ; 196(1): 169-75, 2004 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-15050418

RESUMO

Neuroprotective effect of Ginkgo biloba extract EGb761 in cisplatin (cis-diamminedi-chloroplatinum, or CDDP)-induced peripheral neuropathy was investigated. Swiss albino mice were treated with CDDP, 2 mg/kg ip twice a week for nine times. One group of the animals also received EGb761 in the drinking water at an estimated dosage of 100 mg/kg per day. Two other groups received vehicle (control) or EGb761 only. Development of neuropathy was evaluated with changes in sensory nerve conduction velocity (NCV). Following the treatments, dorsal root ganglia (DRGs) were microscopically examined and some were cultured for 3 days. EGb761 proved effective in preventing the reduction in NCV (P < 0.0001) caused by CDDP. CDDP caused a decrease in the number of migrating cells (P < 0.01) and in the length of outgrowing axons (P < 0.01) while EGb761 treatment prevented the latter. CDDP led to smaller nuclear and somatic sizes in neurons (P < 0.01), while with EGb761 co-administration, both were close to control values. Animals having EGb761 only had similar results with controls. In conclusion, EGb761 was found to be effective in preventing some functional and morphological deteriorations in CDDP-induced peripheral neuropathy.


Assuntos
Cisplatino/toxicidade , Gânglios Espinais/efeitos dos fármacos , Ginkgo biloba , Fármacos Neuroprotetores/farmacologia , Doenças do Sistema Nervoso Periférico/prevenção & controle , Extratos Vegetais/farmacologia , Administração Oral , Animais , Axônios/efeitos dos fármacos , Axônios/patologia , Modelos Animais de Doenças , Estimulação Elétrica , Eletrodos , Feminino , Gânglios Espinais/patologia , Gânglios Espinais/fisiologia , Injeções Intraperitoneais , Camundongos , Microscopia de Fluorescência , Condução Nervosa/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Neurônios/patologia , Doenças do Sistema Nervoso Periférico/induzido quimicamente , Doenças do Sistema Nervoso Periférico/patologia
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