RESUMEN
Diabetes Mellitus (DM) is associated with an increased susceptibility to various infections, which might be attributed to changes in immune response owing to chronic hyperglycemia. Nucleoside triphosphate diphosphohydrolase (NTPDase), 5'-nucleotidase, and adenosine deaminase (ADA) are important enzymes involved in the generation of anti-aggregant and anti-inflammatory microenvironments. The aim of this study was to evaluate the effect of gallic acid (GA) on the hematological parameters and ectonucleotidase activities in platelets, lymphocytes, and serum of diabetic rats. Experimental rats were categorized into 4 groups: (i) control -saline, (ii) control - GA, (iii) diabetic -saline, and (iv) diabetic - GA. One week after induction of DM using streptozotocin (65â¯mg/kg), GA (30â¯mg/kg) or saline was orally administered to the rats for 21 days. Our results demonstrated that the concentration of mean corpuscular hemoglobin was decreased, whereas that of red cell distribution was increased in the diabetic group, however, GA could revert these alterations. Moreover, in diabetic rats, GA reverted the increase in ATP and ADP hydrolysis and ADA activity in lymphocytes, and it prevented the increase in NTPDase and ADA activities in platelets. A decrease in ATP hydrolysis and an increase in ADP and AMP hydrolysis were observed in the serum of diabetic rats; however, GA treatment could solely revert changes in ATP hydrolysis. Our study suggests that GA exhibits beneficial effects on immuno- and thrombo-regulatory responses in DM and that these effects may be related to the modulation of purinergic signaling.
Asunto(s)
Plaquetas/metabolismo , Diabetes Mellitus Experimental/sangre , Ácido Gálico/farmacología , Linfocitos/metabolismo , Nucleótidos de Purina/metabolismo , Suero/metabolismo , Animales , Plaquetas/efectos de los fármacos , Diabetes Mellitus Experimental/tratamiento farmacológico , Ácido Gálico/uso terapéutico , Linfocitos/efectos de los fármacos , Masculino , Agregación Plaquetaria/efectos de los fármacos , Agregación Plaquetaria/fisiología , Nucleótidos de Purina/agonistas , Nucleótidos de Purina/antagonistas & inhibidores , Ratas , Ratas Wistar , Suero/efectos de los fármacos , Transducción de Señal/efectos de los fármacos , Transducción de Señal/fisiologíaRESUMEN
Diabetes mellitus (DM) is characterised by hyperglycaemia associated with the increase of oxidative stress. Gallic acid has potent antioxidant properties. The aim of this study was to evaluate the effect of gallic acid on the biochemical, histological and oxidative stress parameters in the liver and kidney of diabetic rats. Male rats were divided in groups: control, gallic acid, diabetic and diabetic plus gallic acid. DM was induced in the animals by intraperitoneal injection of streptozotocin (65mg/kg). Gallic acid (30mg/kg) was administered orally for 21days. Our results showed an increase in reactive species levels and lipid peroxidation, and a decrease in activity of the enzymes superoxide dismutase and delta-aminolevulinic acid dehydratase in the liver and kidney of the diabetic animals (P<0.05). Gallic acid treatment showed protective effects in these parameters evaluated, and also prevented a decrease in the activity of catalase and glutathione S-transferase, and vitamin C levels in the liver of diabetic rats. In addition, gallic acid reduced the number of nuclei and increased the area of the core in hepatic tissue, and increased the glomerular area in renal tissue. These results indicate that gallic acid can protect against oxidative stress-induced damage in the diabetic state.
Asunto(s)
Diabetes Mellitus Experimental/tratamiento farmacológico , Diabetes Mellitus Experimental/enzimología , Ácido Gálico/uso terapéutico , Riñón/patología , Hígado/patología , Estrés Oxidativo , Porfobilinógeno Sintasa/metabolismo , Animales , Glucemia/metabolismo , Peso Corporal/efectos de los fármacos , Catalasa/metabolismo , Diabetes Mellitus Experimental/sangre , Diabetes Mellitus Experimental/patología , Ácido Gálico/química , Ácido Gálico/farmacología , Glutatión Transferasa/metabolismo , Hepatocitos/efectos de los fármacos , Hepatocitos/patología , Riñón/efectos de los fármacos , Riñón/enzimología , Peroxidación de Lípido/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/enzimología , Masculino , Estrés Oxidativo/efectos de los fármacos , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo , Estreptozocina , Superóxido Dismutasa/metabolismo , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismoRESUMEN
In the present study, we investigated the efficiency of rosmarinic acid (RA) in preventing the alteration of oxidative parameters in the liver and kidney of diabetic rats induced by streptozotocin (STZ). The animals were divided into six groups (n = 8): control, ethanol, RA 10 mg/kg, diabetic, diabetic/ethanol, and diabetic/RA 10 mg/kg. After 3 weeks of treatment, we found that TBARS levels in liver and kidney were significantly increased in the diabetic/saline group and the administration of RA prevented this increase in the liver and kidney (P < 0.05). Diabetes caused a significant decrease in the activity of superoxide dismutase (SOD) and catalase (CAT) in the diabetes/saline group (P < 0.05). However, the treatment with 10 mg/kg RA (antioxidant) prevented this alteration in SOD and CAT activity in the diabetic RA group (P < 0.05). In addition, RA reverses the decrease in ascorbic acid and non-protein-thiol (NPSH) levels in diabetic rats. The treatment with RA also prevented the decrease in the Delta-aminolevulinic acid dehydratase (ALA-D) activity in the liver and kidney of diabetic rats. Furthermore, RA did not have any effect on glycemic levels. These results indicate that RA effectively reduced the oxidative stress induced by STZ, suggesting that RA is a potential candidate for the prevention and treatment of pathological conditions in diabetic models.
Asunto(s)
Antioxidantes/farmacología , Cinamatos/farmacología , Depsidos/farmacología , Diabetes Mellitus Experimental/tratamiento farmacológico , Riñón/metabolismo , Hígado/metabolismo , Animales , Antioxidantes/uso terapéutico , Ácido Ascórbico/metabolismo , Biomarcadores/metabolismo , Glucemia , Cinamatos/uso terapéutico , Depsidos/uso terapéutico , Diabetes Mellitus Experimental/inducido químicamente , Diabetes Mellitus Experimental/metabolismo , Evaluación Preclínica de Medicamentos , Riñón/efectos de los fármacos , Hígado/efectos de los fármacos , Masculino , Malondialdehído/metabolismo , Estrés Oxidativo , Ratas Wistar , Estreptozocina , Superóxido Dismutasa/metabolismo , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo , Ácido RosmarínicoRESUMEN
Diabetes is associated with long-term complications in the brain and reduced cognitive ability. Vitamin D3 (VD3 ) appears to be involved in the amelioration of hyperglycaemia in streptozotocin (STZ)-induced diabetic rats. Our aim was to analyse the potential of VD3 in avoiding brain damage through evaluation of acetylcholinesterase (AChE), Na(+) K(+) -adenosine triphosphatase (ATPase) and delta aminolevulinate dehydratase (δ-ALA-D) activities and thiobarbituric acid reactive substance (TBARS) levels from cerebral cortex, as well as memory in STZ-induced diabetic rats. Animals were divided into eight groups (n = 5): control/saline, control/metformin (Metf), control/VD3 , control/Metf + VD3 , diabetic/saline, diabetic/Metf, diabetic/VD3 and diabetic/Metf + VD3 . Thirty days after treatment, animals were submitted to contextual fear-conditioning and open-field behavioural tests, after which they were sacrificed and the cerebral cortex was dissected. Our results demonstrate a significant memory deficit, an increase in AChE activity and TBARS levels and a decrease in δ-ALA-D and Na(+) K(+) -ATPase activities in diabetic rats when compared with the controls. Treatment of diabetic rats with Metf and VD3 prevented the increase in AChE activity when compared with the diabetic/saline group. In treated diabetic rats, the decrease in Na(+) K(+) -ATPase was reverted when compared with non-treated rats, but the increase in δ-ALA-D activity was not. VD3 prevented diabetes-induced TBARS level and improved memory. Our results show that VD3 can avoid cognitive deficit through prevention of changes in important enzymes such as Na(+) K(+) -ATPase and AChE in cerebral cortex in type 1 diabetic rats.