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1.
Chinese journal of integrative medicine ; (12): 262-268, 2012.
Artículo en Inglés | WPRIM | ID: wpr-289672

RESUMEN

<p><b>OBJECTIVE</b>To investigate the therapeutic effects of Ping-tang Recipe (, PTR) on high-fat diet (HFD)-induced insulin resistance and non-alcoholic fatty liver disease (NAFLD), and to elucidate the underlying mechanisms.</p><p><b>METHODS</b>Forty male SD rats were included in the study. Ten rats were fed on normal diet as normal control, and thirty rats were fed on HFD for 8 weeks to induce obesity, followed with low dose (0.42 g/kg) or high dose (0.84 g/kg) of PTR or vehicle for 8 weeks with 10 animals for each group. Glucose metabolism and insulin sensitivity were evaluated by oral glucose tolerance test and insulin tolerance test. Hepatic steatosis was measured by immunohistochemistry. Liver lipid metabolic genes were analyzed by quantitative real-time polymerase chain reaction, while AMP-activated protein kinase (AMPK) expression was examined by Western blot.</p><p><b>RESULTS</b>Rats fed on HFD developed abdominal obesity, insulin resistance and NAFLD. PTR treatment reduced visceral fat (peri-epididymal and peri-renal) accumulation, improved glucose metabolism, and attenuated hepatic steatosis. The expressions of the key lipolytic regulating genes, including peroxisome proliferators-activated receptor γ co-activator 1α (PGC-1α), peroxisome proliferator-activated receptor γ (PRAR-γ) and α (PRAR-α), were up-regulated (P<0.05 or P<0.01), while the expressions of lipogenic genes such as sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and liver fatty acid-binding protein (L-FABP) were down-regulated (P<0.05 or P<0.01). In addition, PTR activated AMPK and promoted acetyl-CoA carboxylase phosphorylation in the liver.</p><p><b>CONCLUSIONS</b>PTR improves insulin resistance and reverse hepatic steatosis in the rat model of HFD-induced obesity through promotion of lipolysis and reduction of lipogenesis, which involves the AMPK signaling pathway, thus representing a new therapeutic intervention for obesity related insulin resistance and NAFLD.</p>


Asunto(s)
Animales , Masculino , Ratas , Proteínas Quinasas Activadas por AMP , Metabolismo , Peso Corporal , Dieta Alta en Grasa , Medicamentos Herbarios Chinos , Farmacología , Usos Terapéuticos , Hígado Graso , Sangre , Regulación de la Expresión Génica , Glucosa , Metabolismo , Prueba de Tolerancia a la Glucosa , Resistencia a la Insulina , Grasa Intraabdominal , Patología , Lipogénesis , Lipólisis , Hígado , Patología , Obesidad , Sangre , ARN Mensajero , Genética , Metabolismo , Ratas Sprague-Dawley , Triglicéridos , Metabolismo
2.
Chinese Journal of Integrated Traditional and Western Medicine ; (12): 433-435, 2003.
Artículo en Chino | WPRIM | ID: wpr-240938

RESUMEN

<p><b>OBJECTIVE</b>To study the characteristics of cell apoptosis in patients of chronic gastritis with different tongue pictures and its mechanism of formation.</p><p><b>METHODS</b>The tongue picture, apoptosis index (AI) of lingual epithelial cells, apoptosis related gene proteins, such as p53, Bcl-2 and Fas in 109 patients of chronic superficial gastritis were observed.</p><p><b>RESULTS</b>AI was different in patients with different tongue proper and tongue coating, those with pale white tongue and white thick coating had the maximum value of AI. (2) The p53, Bcl-2 and Fas expression positive rates in patients with different tongue pictures had corresponding changes, which were related not only with color of tongue, but also with color and thickness of tongue coating.</p><p><b>CONCLUSION</b>The formation of tongue picture is closely related with cell apoptosis, p53, Bcl-2 and Fas take part in the regulation of cell apoptosis, which constitute together the cytologic basis of tongue picture in the disease.</p>


Asunto(s)
Adolescente , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Apoptosis , Enfermedad Crónica , Gastritis , Metabolismo , Patología , Medicina Tradicional China , Proteínas Proto-Oncogénicas c-bcl-2 , Genética , Lengua , Patología , Proteína p53 Supresora de Tumor , Genética , Receptor fas , Genética
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