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1.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 46(1): 51-6, 2015 Jan.
Artículo en Zh | MEDLINE | ID: mdl-25807796

RESUMEN

OBJECTIVE: To investigate the effect of Shenxiong Huayu capsule on the expression of hippocampal CA1 recombinant protein A (small GTP binding protein A, RHOA) and ROCK-2 (RHO associated protein kinase-2, ROCK-II). METHODS: Clean SD male rats (n=96), divided into three groups with 32 rats for each group, gavage was applied 7 days before modeling until the morning of the day to put to death. The groups included the normal control group (normal saline), global cerebral ischemia model group (normal saline) and Shenxiong Huayu capsule+global cerebral ischemia group (Shenxiong Huayu capsule 0.048 g/kg, was dissolved in 0.5 mL double distilled water, once a day, orally 0.3 mL/100 g). Modified Pulsinelli four-vessel occlusion model was constructed in global cerebral ischemia model and Shenxiong Huayu treatment groups and at 1, 3, 7, 14 d after successful modeling, water maze learning test was applied to evaluate the memory abilities of different groups, histopathological changes in HE staining, expression and protein content of RHOA and ROCK-II in immunohistochemical staining and Western blot was observed. RESULTS: At each time point, escape latency in model group was prolonged (P<0.05) when compared with that in normal control group, and that in Shenxiong Huayu was shorter (P<0.05) than that of model group, but still longer (P<0.05) than that of normal control group. HE staining showed that, compared with the normal group, model hippocampal CA1 reduced gradually from 1 d to 14 d; an increased survival neurons (P<0.05) in Shenxiong Huayu treatment group at each time points was observed, but still less than that in normal group (P<0.05); immunohistochemistry and Western blot analysis demonstrated that the expression of RHOA and ROCK-II in normal control group was not obvious, in model group was decreased after an initial increasing, and that in Shenxiong Huayu treatment group was lower than that of model group (P<0.05), but still higher than that in normal group (P<0.05). CONCLUSION: Shenxiong Huayu capsule improve neuronal damage induced by global ischemia, decreased the expression of hippocampal CA1 region of RHOA and ROCK-II.


Asunto(s)
Isquemia Encefálica/metabolismo , Región CA1 Hipocampal/metabolismo , Medicamentos Herbarios Chinos/farmacología , Daño por Reperfusión , Quinasas Asociadas a rho/metabolismo , Proteína de Unión al GTP rhoA/metabolismo , Animales , Región CA1 Hipocampal/efectos de los fármacos , Masculino , Aprendizaje por Laberinto , Memoria , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Ratas , Ratas Sprague-Dawley
2.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 42(2): 237-40, 2011 Mar.
Artículo en Zh | MEDLINE | ID: mdl-21500562

RESUMEN

OBJECTIVE: To investigate the effect of sleep deprivation (SD) on the expression of p38Mitogen-activated protein kinase (p38MAPK) phosphorylation in the rat hippocampus. METHODS: Male Sprague-Dawley rats (n=60) were divided randomly into control and sleep deprivation groups. The sleep deprivation models were established with the modified multiple platform methods. At 1 d, 3 d, 5 d, and 7 d after sleep deprivations, changes of neuron morphous in the hippocampal region of the rats were observed by HE staining. The expression of p38MAPK phosphorylation was detected by immunohistochemistry and Western blot. The learning-memory function was tested with Morris water maze and 4-PTT dry path maze. RESULTS: More obvious neuronal morphous damages, increased p38MAPK phosphorylation cells and p38MAPK phosphorylation expression, and decreased learning-memory function were found in the rats subject to sleep deprivation than those in the control. The changes were enhanced with the length of sleep deprivation. CONCLUSION: p38MAPK can be activated by sleep deprivation, which mediates the process of neuronal injury.


Asunto(s)
Hipocampo/metabolismo , Hipocampo/patología , Privación de Sueño/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo , Animales , Masculino , Fosforilación , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Privación de Sueño/patología
3.
Int J Pharm ; 360(1-2): 58-64, 2008 Aug 06.
Artículo en Inglés | MEDLINE | ID: mdl-18502064

RESUMEN

Ultrafine gemfibrozil (GEM) was prepared by reactive precipitation process in which methyl cellulose (MC) was employed to inhibit the growth and the agglomeration of particles. The impact of NaOH concentrations on bulk GEM consumption was explored. The effects of H2SO4 concentrations and the drying methods on the particle size and morphology were also discussed. The produced ultrafine powders were characterized by scanning electron microscopy (SEM), X-ray diffraction (XRD), Fourier transform infrared (FT-IR) spectroscopy, specific surface area analysis and dissolution test. XRD patterns and FT-IR spectra showed that the as-obtained ultrafine GEM was a crystalline powder with the structure and components similar to those of bulk GEM. The ultrafine GEM had a mean particle size of about 1.25 microm with a narrow distribution from 0.6 to 3 microm. The specific surface area reached up to 11.01 m2/g, which was about 6 times as large as that of bulk GEM. In the dissolution tests, about 91.2% of ultrafine GEM was dissolved after 120 min, while there was only 23.6% of bulk GEM dissolved, proving that the dissolution property of ultrafine GEM was significantly enhanced when compared to commercial GEM owing to a decreased particle size and an increased specific surface area.


Asunto(s)
Gemfibrozilo/administración & dosificación , Gemfibrozilo/química , Hipolipemiantes/administración & dosificación , Hipolipemiantes/química , Química Farmacéutica , Cromatografía Líquida de Alta Presión , Desecación , Excipientes , Microscopía Electrónica de Rastreo , Tamaño de la Partícula , Polvos , Hidróxido de Sodio/química , Solubilidad , Espectroscopía Infrarroja por Transformada de Fourier , Ácidos Sulfúricos/química , Difracción de Rayos X
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