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1.
Ann Hepatol ; 10(2): 207-15, 2011.
Artículo en Inglés | MEDLINE | ID: mdl-21502683

RESUMEN

This study examined the possible hepatoprotective effect of aminoguanidine in comparison with silymarin and investigated the possible beneficial effects of the combination of aminoguanidine and silymarin on CCL4-induced liver fibrosis. Male Wister albino rats were randomly divided into five groups (10 rats/group). Group I included control rats injected only with liquid paraffin and saline; group II represents CCL(4) control (injected with CCL(4) 3 times a week for 6 weeks in a dose of 25µl/100gm.b.w i.p, diluted 1:6 with liquid paraffin); group III treated with aminoguanidine (100 mg/kg); group IV was given silymarin (100 mg/kg); group V was given aminoguanidine (100 mg/kg) and silymarin (100 mg/kg). Fibrosis was depicted histologically and biochemically. CCL4 increased serum liver enzymes (ALT, AST, and ALP), lactate dehydrogenase (LDH), level of nitric oxide (NO), tumor necrosis factor alpha (TNFα) and liver malondialdehyde content (MDA), collagen fiber percent and decreased liver reduced glutathione (GSH) content as endogenous antioxidant. Histopathological changes induced by CCL4 include regenerative nodules, deteriorated parenchyma; the lobules were infiltrated with fat and structurally altered. Aminoguanidine, silymarin and their combination reduced these changes and attenuated the pathological effects of CCL(4) induced liver injury. The combination of both drugs was better than each drug alone. It is concluded that aminoguanidine has protective effect against CCL(4) induced hepatoxicity via its iNOS inhibition and antioxidant effects. In addition, the combination of AG with silymarin has more potent hepatoprotective effect than each drug alone.


Asunto(s)
Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Inhibidores Enzimáticos/farmacología , Guanidinas/farmacología , Sustancias Protectoras/farmacología , Silimarina/farmacología , Animales , Tetracloruro de Carbono/toxicidad , Muerte Celular/efectos de los fármacos , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Colágeno/metabolismo , Sinergismo Farmacológico , Hepatocitos/efectos de los fármacos , Hepatocitos/patología , Hepatocitos/ultraestructura , Cirrosis Hepática/tratamiento farmacológico , Cirrosis Hepática/metabolismo , Cirrosis Hepática/patología , Masculino , Microscopía Electrónica , Óxido Nítrico Sintasa de Tipo II/metabolismo , Ratas , Ratas Wistar , Factor de Necrosis Tumoral alfa/metabolismo
2.
Food Chem Toxicol ; 49(5): 1129-40, 2011 May.
Artículo en Inglés | MEDLINE | ID: mdl-21310207

RESUMEN

This study was conducted to investigate the effect of curcumin, obtained from Curcuma longa, in comparison with rosiglitazone on the progression of insulin resistance and type 2 diabetes mellitus (T2DM) and the mechanisms underlying this effect. Insulin resistance and T2DM was induced in male Sprague Dawley rats by high fat diet (HFD) feeding for 60 and for 75 days representing two regimens of the study, protection and treatment. Prophylactic oral administration of curcumin (80 mg/kg), rosiglitazone (1 mg/kg), their combination, or vehicle (in control groups) was started along with HFD feeding in different groups. Treatment is achieved by oral administration of the previously mentioned agents in the last 15 days of HFD feeding after induction of insulin resistance and T2DM in rats. Curcumin showed an anti-hyperglycemic effect and improved insulin sensitivity, and this action may be attributed at least in part to its anti-inflammatory properties as evident by attenuating TNF-α levels in HFD fed rats, and its anti-lipolytic effect as evident by attenuating plasma free fatty acids. The curcumin effects are comparable to those of rosiglitazone, which indicate that they may act similarly. Finally we can say that, curcumin could be a beneficial adjuvant therapy in patients with T2DM.


Asunto(s)
Curcumina/farmacología , Grasas de la Dieta/administración & dosificación , Ácidos Grasos no Esterificados/sangre , Hipoglucemiantes/farmacología , Factor de Necrosis Tumoral alfa/sangre , Administración Oral , Análisis de Varianza , Animales , Glucemia/análisis , Composición Corporal , Diabetes Mellitus Tipo 2/sangre , Diabetes Mellitus Tipo 2/metabolismo , Prueba de Tolerancia a la Glucosa , Insulina/sangre , Resistencia a la Insulina , Masculino , Ratas , Ratas Sprague-Dawley , Rosiglitazona , Tiazolidinedionas/farmacología , Triglicéridos/sangre
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