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Medicinas Complementárias
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1.
Ocul Immunol Inflamm ; 28(6): 888-897, 2020 Aug 17.
Artículo en Inglés | MEDLINE | ID: mdl-31429629

RESUMEN

INTRODUCTION: It was aimed to evaluate the efficacy of two tea tree oil (TTO)-based cleansing gels in chronic blepharitis patients. METHODS: Group-1 (basic gel containing 3%(w/w)-TTO) included 50 eyes of 25 patients and group-2 (advanced gel containing 3%(w/w)-TTO plus essential oils and vitamins) included 48 eyes of 24 patients. Ocular Surface Disease Index (OSDI), tear breakup time (TBUT), ocular surface staining pattern, Schirmer's test, impression cytology, Demodex presence and TNF-α, IL-6, IL-1ß levels were evaluated at the first visit and 1 month after treatment. RESULTS: In both groups, the mean OSDI score decreased (p1:0.001, p2:0.001), TBUT increased (p1:0.002, p2:0.004). In group-1, Demodex presence decreased from 42% to 27.8%; in group-2 from 54.2% to 20.6% (p1:0.302, p2:0.004). IL-1ß and IL-6 decreased in group-2 (p1:0.002, p2:0.050). TNF-α decreased in both groups (p1:0.001, p2:0.001). CONCLUSION: Both formulations improved ocular surface parameters. Group 2 showed more reduction in tear cytokines and Demodex count.


Asunto(s)
Antiinfecciosos Locales/uso terapéutico , Blefaritis/tratamiento farmacológico , Aceite de Árbol de Té/uso terapéutico , Adulto , Animales , Antiinfecciosos Locales/efectos adversos , Blefaritis/metabolismo , Blefaritis/parasitología , Enfermedad Crónica , Método Doble Ciego , Ensayo de Inmunoadsorción Enzimática , Proteínas del Ojo/metabolismo , Pestañas/parasitología , Femenino , Geles , Humanos , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Masculino , Persona de Mediana Edad , Ácaros , Preparaciones Farmacéuticas , Aceite de Árbol de Té/efectos adversos , Lágrimas/metabolismo , Resultado del Tratamiento , Factor de Necrosis Tumoral alfa/metabolismo
2.
J Int Adv Otol ; 12(2): 177-183, 2016 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-27487360

RESUMEN

OBJECTIVE: The aim of our study was to investigate the effects Korean Red Ginseng (KRG) on cisplatin (CDDP) ototoxicity in vivo and in vitro. MATERIALS AND METHODS: The first part of the study was conducted on the House Ear Institute-Organ of Corti 1 (HEI-OC1) cell line. Cells were treated with CDDP, KRG, and their combination for 24 h. Cell viability, apoptosis, and the expression of 84 apoptosis-related genes were analyzed. In the second part of the study, 30 Wistar albino rats were divided into five groups. Baseline distortion product otoacoustic emissions (DPOAEs) and auditory brainstem response (ABR) measurements were obtained. In groups I, II, and III, only saline, KRG, and CDDP, respectively, were given. In group IV, 500 mg/kg KRG and in group V, 150 mg/kg of KRG were administered for 10 days. In groups III, IV, and V, 16 mg/kg CDDP injections were administered on day 11. On day 14, final DPOAEs and ABR measurements were completed. The rats were then sacrificed, and their inner ear structures were evaluated by transmission electron microscopy. RESULTS: In the first part of the study, pretreatment with 1 mg/mL KRG protected cells from CDDP ototoxicity. This protection was mainly due to a decline in apoptotic gene expression and an increase in antiapoptotic gene expression. In the in vivo part of the study, we found that both KRG doses had otoprotective effects. This protection was more prominent at the lower dose, especially on the spiral ganglion and the brainstem. CONCLUSION: KRG was shown to be an otoprotective agent against CDDP-induced ototoxicity both in vivo and in vitro.


Asunto(s)
Antineoplásicos/efectos adversos , Cisplatino/efectos adversos , Pérdida Auditiva/inducido químicamente , Pérdida Auditiva/prevención & control , Panax , Fitoterapia , Animales , Apoptosis , Técnicas de Cultivo de Célula , Supervivencia Celular , Pérdida Auditiva/patología , Ratas , Ratas Wistar
3.
Toxicol Ind Health ; 32(1): 106-17, 2016 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-24021433

RESUMEN

The herbicide itself and the degradation products are highly toxic on biological systems. The aim of this study is to investigate the potential toxic effects of trifluralin (TRF) on the urinary system of male rats and to investigate the protective effects of resveratrol (RSV) in TRF-induced urinary system damage. A total of 35 male Wistar rats were randomly divided into: (1) control group, (2) sham group, (3) low dose TRF group (0.8 g/kg/day), (4) high dose TRF group (2 g/kg/day) and (5) high dose TRF + RSV group 10 mg/kg/day. RSV was administered for 21 days by intragastric gavage at a dose of 10 mg/kg/day after induction of TRF. Kidney, ureter and urinary bladder tissue was examined using light microscopy and ultrastructurally. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling was performed to detect apoptosis. Superoxide dismutase (SOD), glutathion peroxidase (GPx) and malondialdehyde (MDA) levels were also evaluated biochemically for oxidative stress parameters. Histological evaluation showed that TRF increases apoptosis and oxidative stress, causes histological tissue damages and biochemical changes in the kidneys but does not cause any damage to the ureter and bladder. Treatment with RSV significantly attenuated tissue damage in the urinary system of rats. Apopitotic cells were significantly decreased in the treatment group. Additionally, treatment with RSV decreased SOD and GPx levels and increased MDA levels in the kidney tissue of animals subjected to TRF. These results show that RSV can significantly minimize histological damage and biochemical differences in treating TRF-induced kidney injury in rats.


Asunto(s)
Antioxidantes/farmacología , Estilbenos/farmacología , Trifluralina/toxicidad , Sistema Urinario/efectos de los fármacos , Animales , Apoptosis/efectos de los fármacos , Peso Corporal , Relación Dosis-Respuesta a Droga , Glutatión Peroxidasa/metabolismo , Etiquetado Corte-Fin in Situ , Enfermedades Renales/inducido químicamente , Enfermedades Renales/tratamiento farmacológico , Masculino , Malondialdehído/metabolismo , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Wistar , Resveratrol , Superóxido Dismutasa/metabolismo , Sistema Urinario/metabolismo , Sistema Urinario/patología
4.
Allergy Asthma Proc ; 30(2): 186-91, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-19118503

RESUMEN

Platelet-activating factor (PAF) is an inflammatory mediator involved in the pathophysiology of asthma, suggesting a therapy antagonizing its effects may play a role in the disease treatment. The aim of the study was to determine the effects of Ginkgo biloba, a PAF antagonist, on lung histology. Thirty-five BALB/c mice were divided into five groups; A, B, C, D, and the control. All mice except controls were sensitized and challenged with ovalbumin. Mice in group A (placebo) received saline; group B received G. biloba, 100 mg/kg; group C received G. biloba, 150 mg/kg; and group D received dexamethasone, 1 mg/kg via orogastric gavage for 7 consecutive days. Chronic structural changes and airway remodeling were evaluated by using light and electron microscopy in all groups. Evaluation of lung histology indicated that the number of goblet cells, mast cells, thicknesses of epithelium, and basement membrane were significantly improved in groups B and C when compared with group A. There was no statistically significant difference in thicknesses of subepithelial smooth muscle between groups A, B, and C. When doses of G. biloba were compared with each other, only the number of goblet cells was significantly lower in group C than in group B. When G. biloba and dexamethasone groups were compared with each other, thicknesses of basement membrane and subepithelial smooth muscle were found to be lower in group D than in groups B and C. G. biloba alleviates all established chronic histological changes of lung except smooth muscle thickness in a mouse model of asthma.


Asunto(s)
Asma/tratamiento farmacológico , Asma/patología , Ginkgo biloba , Pulmón/efectos de los fármacos , Pulmón/patología , Fitoterapia , Extractos Vegetales/uso terapéutico , Mucosa Respiratoria/efectos de los fármacos , Mucosa Respiratoria/patología , Animales , Asma/inmunología , Enfermedad Crónica , Modelos Animales de Enfermedad , Inmunización Secundaria , Inyecciones Intraperitoneales , Pulmón/inmunología , Masculino , Ratones , Ratones Endogámicos BALB C , Ovalbúmina/inmunología , Hojas de la Planta , Factor de Activación Plaquetaria/antagonistas & inhibidores , Mucosa Respiratoria/inmunología
5.
Neurosci Lett ; 438(3): 265-9, 2008 Jun 27.
Artículo en Inglés | MEDLINE | ID: mdl-18490106

RESUMEN

It is known that the brain tissue is extremely sensitive to ischemia-reperfusion (IR) injury and therefore, brain ischemia and consecutive reperfusion result in neural damage and apoptosis. The proinflammatory cytokines such as tumor necrosis factor alfa (TNF-alpha) and interleukin-1 beta (IL-1beta) are produced during neurological disorders including cerebral ischemia. On the other hand, nerve growth factor (NGF), which is essential for the differentiation, survival and functions of neuronal cells in the central nervous system, regulate neuronal development through cell survival and cell death signaling. In the present study, we aimed to investigate the effect of selenium (Se) on prefrontal cortex and hippocampal damage in rats subjected to cerebral IR injury. Selenium was injected intraperitoneally at the doses of 0.625 mg/(kg day) after induction of IR injury. Prefrontal cortex and hippocampal damage was examined by cresyl-violet staining. Apostain and caspase-3 immune staining were used to detect apoptosis. TNF-alpha, IL-1beta and NGF levels were also evaluated. Histopathological evaluation showed that treatment with selenium after ischemia significantly attenuated IR-induced neuronal death in prefrontal cortex and hippocampal CA1 regions of rats. Apoptotic cells stained with apostain and caspase-3 were significantly decreased in treatment group when compared with the IR group. Additionally, treatment with selenium decreased the TNF-alpha and IL-1beta levels and increased the NGF levels in prefrontal cortex and hippocampal tissue of animals subjected to IR. The present results suggest that selenium is potentially a beneficial agent in treating IR-induced brain injury in rats.


Asunto(s)
Antioxidantes/uso terapéutico , Corteza Prefrontal/efectos de los fármacos , Daño por Reperfusión/tratamiento farmacológico , Daño por Reperfusión/patología , Selenio/uso terapéutico , Animales , Caspasa 3/metabolismo , Modelos Animales de Enfermedad , Hipocampo/efectos de los fármacos , Etiquetado Corte-Fin in Situ , Interleucina-1beta , Masculino , Factores de Crecimiento Nervioso , Ratas , Ratas Wistar , Factor de Necrosis Tumoral alfa
6.
Biol Trace Elem Res ; 95(1): 87-94, 2003 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-14555802

RESUMEN

Thirty adult male mice were divided into three groups. The animals in group I were used as controls and drank only water during the entire period of experimentation. Group II animals drank water containing 1.5 g/100 mL zinc as ZnSO4, and group III animals received 2.5 g/100 mL zinc. After 3 wk supplementation with high doses of zinc, the animals were killed and the livers were removed and examined by electron microscopic techniques. After the supplementation period, the animals in groups II and II showed various degrees of degenerative changes in the hepatocytes, such as increased size and the presence of spaces and an abundance of lipid globules in the cytoplasm. The mitochondria showed a crystalline appearance, a diluted matrix, and dense aggregations. Some smooth endoplasmic reticulum tubules showed dilation and were filled with a dense substance. None of these changes were present in the group I control animals.


Asunto(s)
Hígado/efectos de los fármacos , Hígado/ultraestructura , Zinc/envenenamiento , Animales , Enfermedad Hepática Inducida por Sustancias y Drogas , Sobredosis de Droga , Hepatocitos/efectos de los fármacos , Hepatocitos/patología , Hepatocitos/ultraestructura , Hígado/citología , Hígado/patología , Hepatopatías/patología , Masculino , Ratones , Ratones Endogámicos BALB C , Microscopía Electrónica , Orgánulos/efectos de los fármacos , Orgánulos/patología , Orgánulos/ultraestructura
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