RESUMEN
This study was set to investigate the effect of gum Arabic (G.A.) on diabetic kidney disease. We divided sixty male Sprague rats randomly into six groups. Normal control, normal rats treated with G.A., untreated diabetic rats, diabetic rats treated with insulin, diabetic rats treated with G.A., and diabetic rats treated with both insulin and G.A. Diabetes was induced by a single intraperitoneal injection of STZ. Forty eight hr post injections. Insulin was injected subcutaneously (1.6/IU/100g/day). We provided G.A. in drinking water (10 %w/ v).). At the end of the twelve weeks, blood was drawn for measurement of blood glucose, glycosylated hemoglobin (HbA1C), serum lipids, serum creatinine, and blood urea. Renal tissue oxidative stress (O.S.) was assessed by measuring the activities of superoxide dismutase (SOD) and catalase (CAT), and the concentrations of reduced glutathione (GSH) and malondialdehyde (MDA). For histological assessments, sections from segments of kidneys were processed and stained with hematoxylin and eosin (H&E) for assessment under the light microscope. STZinduced diabetes caused an elevation of blood glucose, HbA1c, urea and creatinine, triglycerides LDL and cholesterol, MDA with reduction of HDL, GSH level, and CAT and SOD activities. Histologically, kidneys from diabetic rats showed marked glomerular and tubular changes. Administration of G.A. alone to diabetic rats had a significant hypoglycemic, hypolipidemic, and antioxidant effect, although the levels achieved remained significantly abnormal compared with the untreated group with no effect on urea and creatinine levels. Co-administration of G.A. with insulin reversed the impact of D.M. on all parameters evaluated including the histological changes and led to normal urea and creatinine levels. We concluded that G.A., in combination with insulin, improves chemically-induced diabetes and its renal complications, possibly by modulation of oxidative stress.
En este estudio se evaluó el efecto de la goma arábiga (GA) en la enfermedad renal diabética. Dividimos sesenta ratas macho Sprague Dawley al azar en seis grupos. Control normal, ratas normales tratadas con GA, ratas diabéticas no tratadas, ratas diabéticas tratadas con insulina, ratas diabéticas tratadas con GA y ratas diabéticas tratadas con insulina y GA. La diabetes fue inducida por una sola inyección intraperitoneal de STZ. Cuarenta y ocho horas después se inyectó insulina por vía subcutánea (1,6 / UI / 100 g / día). A los animales se les dió GA en agua potable (10 % p / v)). Al final de las doce semanas, se extrajo sangre para medir la glucosa, la hemoglobina glicosilada (HbA1C), los lípidos en suero, la creatinina en suero y la urea en sangre. El estrés oxidativo del tejido renal (SO) se evaluó midiendo las actividades de la enzima superóxido dismutasa (SOD) y la catalasa (CAT), y las concentraciones de glutatión reducido (GSH) y malondialdehído (MDA). Para las evaluaciones histológicas, se procesaron secciones de segmentos de riñones y se tiñeron con hematoxilina y eosina (H & E) para análisis bajo microscopio óptico. La diabetes inducida por STZ causó una elevación de la glucosa en sangre, HbA1c, urea y creatinina, triglicéridos LDL y colesterol, MDA con reducción de las actividades de HDL, GSH y CAT y SOD. Histológicamente, los riñones de ratas diabéticas mostraron marcados cambios glomerulares y tubulares. La administración de GA solo en las ratas diabéticas tuvo un efecto hipoglucémico, hipolipidémico y antioxidante significativo, aunque los niveles alcanzados permanecieron significativamente anormales en comparación con el grupo no tratado, sin ningún efecto sobre los niveles de urea y creatinina. La dministración conjunta de GA con insulina revirtió el impacto de DM en todos los parámetros evaluados, incluidos los cambios histológicos y condujeron a niveles normales de urea y creatinina. Concluimos que GA en combinación con insulina, mejora la diabetes inducida químicamente y sus complicaciones renales, posiblemente mediante la modulación del estrés oxidativo.
Asunto(s)
Animales , Masculino , Ratas , Nefropatías Diabéticas/prevención & control , Goma Arábiga/administración & dosificación , Antioxidantes/administración & dosificación , Ratas Sprague-Dawley , Estrés Oxidativo/efectos de los fármacos , Diabetes Mellitus Experimental/complicaciones , Diabetes Mellitus Experimental/patología , Diabetes Mellitus Experimental/tratamiento farmacológico , Nefropatías Diabéticas/patología , Goma Arábiga/farmacología , Inyecciones Intraperitoneales , Riñón/efectos de los fármacos , Antioxidantes/farmacologíaRESUMEN
Diabetic nephropathy [DNP] is a chronic renal disease [CRD] and a major cause of illness and premature death in people with diabetes mellitus [DM]. It is the single most important cause of end-stage renal disease in the Western world and accounts for more than a quarter of all end-stage renal diseases. This article reviews the current development in DNP and the therapeutic challenge with particular reference to the role of calcium channel blockers. Moreover, renal ischaemia hastens the progression of DNP. Diltiazem and amlodipine have a tendency to reverse the changed parameters toward normal values but do not affect the biochemical parameters. Generally speaking, diltiazem is better than amlodipine in reversing biochemical and histopathological changes produced by DNP, and captopril reverses most of the changed parameters with the exception of the histopathological changes. These agents have nephroprotective properties and delay the progression of DNP
Asunto(s)
Humanos , Complicaciones de la Diabetes , Bloqueadores de los Canales de Calcio , Amlodipino , Diabetes Mellitus , Diltiazem , Factores de Riesgo , Nefropatías Diabéticas/prevención & control , IsquemiaRESUMEN
Three types of calcium channels have been identified voltage-sensitive, receptor operated [cardiac muscle and vascular smooth muscle] and stretch operated [in some blood vessels] channels. Using electrophysiological and pharmacological techniques, three different types of voltage-gated calcium channels have been identified, namely, L-type [for long lasting, large channels], T-type [for transient, tiny channels] and N-type [for neuronal, neither L nor T]. Many compounds are known to have a calcium channel inhibitory effect. Calcium antagonists, based on the specificity of inhibition of the slow calcium current, can be classified into three groups: Group A: for 90 to 100 percent inhibition of calcium influx without change in the sodium current [verapamil, diltiazem and the dihydropyridines]; Group B: for 50 to 70 percent inhibition of calcium influx current without change in the sodium current [bepridil, cinnarizine and prenylamine] and Group C: for agents exhibiting some inhibition of calcium influx [phenytoin, indomethacin and propranolol]. There is now increasing evidence that, certain calcium channel blockers especially the dihydropyridines are more strongly associated with vasodilation of afferent arterioles than of efferent arterioles and also with increase intraglomerular pressure and albuminuria. Thus they have a beneficial effect in terms of reducing proteinuria and slowing the progression of diabetic renal failure
Asunto(s)
Humanos , Amlodipino/farmacología , Nefropatías Diabéticas/tratamiento farmacológico , Isquemia , Diabetes Mellitus , Diltiazem/farmacología , Bloqueadores de los Canales de Calcio/clasificación , Bloqueadores de los Canales de Calcio/historiaRESUMEN
In this study, the effects of A. nilotica [AAN] in serum glucose, lipids and hepatic functions were evaluated in normal and streptozotocin [STZ]-induced diabetic rats. The experimental animals were divided into four groups: A normal untreated group orally administered a vehicle for three weeks, a normal AAN-treated group received oral daily dose of AAN [58 mg/kg] for three weeks, a diabetic untreated group injected i.p. with STZ [60 mg/kg] and a diabetic AAN- treated group included STZ-induced diabetic rats received a daily oral dose of AAN extract for three weeks. Serum glucose, triglycerides [TG], cholesterol, alanine minotransferase [ALT], and aspartate aminotransferase [AST] were analyzed. Paraffin-embedded liver sections were used for histopathology and detection of polysaccharides contents and immuno expression of the anti-apoptotic protein Bcl-2. STZ-induced diabetic rats showed significant elevation of serum glucose and hepatic markers [ALT and AST] with hepatic cellular swelling, cytoplasmic alterations, nuclear hypertrophy, cellular damage and depleted hepatic polysaccharides. Administration of AAN produced a significant hypoglycemic effect in normal rats and significant decreases in serum glucose, cholesterol and TG in diabetic rats. Also, AAN stimulated the expression of the Bcl-2 protein in the liver of both normal and STZ-induced diabetic rats and prevented the occurrence of hepatic cellular swelling and damage. However, administration of AAN to normal rats in creased insignificantly ALT and AST levels accompanied with few hepatic cellular changes. Moreover, administration of AAN to diabetic rats did not significantly decrease the elevated serum ALT and AST levels