Preventive role of gum Arabic administration on STZ induced diabetic kidney disease in rats; renal antioxidant and histopathological evidence / Función preventiva de la administración de goma arábiga en la enfermedad renal diabética inducida por STZ en ratas; antioxidante renal y evidencia histopatológica

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.

Effects of reduced glutathion and vitamin c on cisplatin-induced hepatotoxicity in rats

Cisplatin [CDDP] is a widely used anticancer drug, however it can produce undesirable side effects such as hepatotoxicity when used at high doses. The aim of the present work to evaluate the protective effect of reduced glutathione [GSH] and vitamin C on CDDP-induced hepatotoxicity. Eighty male Sprague-Dawley rats were divided into eight groups, 10 rats each. Group I, control group. Group II received Cisplatin [7.5 mg /kg, i.p] for 5 consecutive days. Group III received GSH [600 mg/kg /day, i.p]. Group IV received vitamin C [250 mg/kg/day, orally]. Group V received GSH for 15 days then CDDP for 5 days. Group VI administered vitamin C for 15 days then CDDP for 5 days. Group VII administered both GSH and CDDP for 5 days. The last Group [VIII] administered both vitamin C and CDDP for 5 days. Serum alanine aminotransferase [ALT] and aspartate aminotransferase [AST] activities [markers of hepatotoxicity], antioxidants [superoxide dismutase [SOD], glutathione peroxidase [GSHPx], catalase [CAT], glutathione reductase [GSHR] activities and gene expression, glutathione [GSH] content] and lipid peroxidation products [malondialdehyde, MDA] in rat liver tissue were measured. CDDP hepatotoxicity was manifested by an increase in serum ALT and AST, elevation of MDA as well as a decrease in GSH and the activities and gene expression of antioxidant enzymes [SOD, GSHPx, CAT, GSHR] in liver tissues. Serum ALT, AST and hepatic MDA decreased in the combination groups in comparison with the CDDP group. The activities and gene expression of SOD, GSHPx, CAT and GSHR and the GSH concentration increased in the combination groups as compared to the CDDP group. Reduced glutathione and vitamin C either taken before or concomitant with cisplatin attenuated the CDDP hepatotoxicity

Characterization of angiotensin converting enzyme gene polymorphism and risk of different heart diseases

The present work aims to test the association of angiotensin converting enzyme [ACE] gene insertion/ deletion [I/D] polymorphism in patients with myocardial infarction [MI]. The study comprised 79 Egyptian cases with MI. Their mean age was 54.4 +/- 9.9 years including 60 [75%] males and 19 [24.1%] females, 23 [29.1%] were smokers, 21 [26.6%] had a positive family history of MI, 25 cases [31.6%] were diabetic, 16 cases [20.3%] were hyperlipidemic. For comparison, 238 healthy subjects of nearly matched age and sex, with no history of any cardiac diseases were taken as a control group. For all subjects, DNA testing for ACE gene I/D polymorphism was done using PCR amplification to detect both D and I alleles followed by a second run PCR specific for the I allele for cases typed as DD in the first run. Cases had higher frequency of DD [29.1%] and ID [62%] than II [8.9%] genotype with a higher frequency of D allele than I allele [64.4% vs 33.6%]. Compared to controls, cases had significantly higher frequency of ID genotype [62% versus 47.5%, P < 0.05]. Cases with low risk factors had a higher frequency of ID genotype compared to controls [66.7% vs 47.5%, P = 0.002]. The same was, also, found in the high risk group but with a lower level of significance [63.6% vs 47.5%, P = 0.041]. ACE gene polymorphism is probably a risk factor for ischemic heart disease among Egyptian cases particularly if integrated with other environmental and genetic risk factors

N-acetylcysteine attenuates cyclosporine-induced nephrotoxicity in male albino rats

Cyclosporine A [Cs A] is used for the treatment of autoimmune and inflammatory disorders. However, Cs A-induced nephrotoxicity remains an important clinical problem, and oxidative stress has been implicated as a possible responsible mechanism. We assessed the protective ability of N-acetylcysteine [NAC], an antioxidant, against Cs A-induced nephrotoxicity. Thirty adult male albino rats were used to study the effect of cyclosporine [Cs A] and the action of N-acetylcysteine [NAC] on certain renal parameters; Blood Urea Nitrogen [BUN] and creatinine. Malondialdehyde [MDA] and catalase [CAT] levels were used as biomarker for testing the antioxidant potential of the drug. Endothelin-l[ET-l] levels were estimated in plasma. Animals were randomly assigned into three groups. Group I rats as control, group 2 were treated with Cs A and group 3 with Cs A plus NAC. Cs A administration for 21 days produced elevated levels of MDA and decreased in antioxidant enzyme CAT and deteriorated the renal function as assessed by increased serum Blood Urea Nitrogen [BUN] and creatinine. Plasma ET-l was also elevated as compared to control groups. Oral administration of NAC [140 mg/kg/day] significantly attenuated renal dysfunction, reduced elevated levels of MDA, increased the level of CAT and decreased level of ET- 1. These results indicate that NAC produces a protective mechanism against Cs A-induced nephrotoxicity in rats and suggest a role of Cs A for oxidative stress and the nephroprotective role of NAC against Cs A-induced nephrotoxicity in rats

Studying the effect of L-ascorbic acid on oral hypoglycemic drug [gliclazid] in treatment of diabetic albino rats

In this work, thirty adult male albino rats were used to study the effect of L - ascorbic acid on oral hypoglycemic drug [gliclazid] in treatment of diabetic rats. Rats were divided into three equal groups, I, II, III. Rats subjected to induction of diabetes by alloxan 100 mg /kg body weight. Rats showing fasting blood glucose level above 150 mg/dl were selected for the study. Group I received gliclazid 7 mg/Kg body weight Group II received gliclazid 7 mg/kg + L .ascorbic acid [L .A .A] 40 mg/Kg body weight. Group III received gliclazid 7 mg/kg + L .A .A 60 mg/kg body weight. Blood glucose level determined at different time interval after administration of drugs. The study showed that L.A.A produced hypoglycemic effect in a dose dependent manner in diabetic rats. Also, L.A.A/gliclazid produced early onset of action and maintained for long period compared to gliclazid treatment only

potential therapeutic effect of melatonin in reflux esophagitis

Melatonin is synthesized not only in the pineal gland, but also in different organs, the special attention has been directed to the digestive tract where total quantity of melatonin is considerably greater than in the pineal gland. Many drugs were used for the treatment of reflux esophagitis such as omeprazote [a proton pump inhibitor] which is widely used antiulcer drug and has been demonstrated to protect against esophageal mucosal injury. The aim of this study is to evaluate the role of exogenous melatonin in the treatment of reflux esophagitis in human either alone and in combination with omeprazole therapy. 36 persons were divided into 4 groups [control patients with reflux esophagitis treated by melatonin for 4, 6 and 8 weeks, patients with reflux esophagitis treated with omeprazole for same periods, and patients with reflux esophagitis treated with combination of melatonin and omeprazole for same periods]. Each group consisted of 9 persons. Persons were subjected to thorough history taking, clinical examination, investigations [laboratory, encioscopic, record of esophageal motility, pH-metry]. Melatonin has a role in improvement of Gastro-esophageal reflux disease [GERD] either used alone or in combination with omeprazole. Meanwhile, omeprazole [a proton pump inhibitor] alone is better used in treatment of GERD than melatonin alone. The present study showed that oral melatonin is a promising therapeutic agent for the treatment of GERD. It is an effective line of treatment in relieving epigastric pain and heart burn. However, further studies are required to confirm the efficacy and long-term safety of melatonin before it can be recommended for routine clinical use

Mechanism of food additive [monosodium glutamate]- induced obesity a molecular study

There is no question that there is an obesity epidemic in our country, as well as in some other countries. Obesity during pregnancy increases maternal and fetal morbidity and is a risk factor for gestational diabetes and hypertensive disorders of pregnancy. There are many causes of obesity from them the bad use of food additives, the monosodium glutamate is considered one of the most popular food additives. The results of previous studies on the role of monosodium glutamate in developing of obesity are controversial so the aim of this paper is to determine the role of MSG in developing obesity through studying its effect on Ob gene expression and leptin receptor-b gene expression and to determine its effect on some cardiac disease indicators as apo-A[1] and apo-B. We used in this study 60 pregnant female rats which were divided into 2 groups, control group and group supplemented with monosodium glutamate. In all rats, determination of biochemical parameters as serum glucose, insulin, leptin, total lipids, cholesterol HDL, LDL, VLDL, apo A1, apo B, as well as determination of Ob and leptin receptor-b gene expression were done. Our results indicated that the administration of monosodium glutamate is accompanied with increase of Ob gene expression, leptin, insulin, lipoprotein B, lipogram, glucose and decrease of brain leptin receptor-b gene expression, lipoprotein lipase activity and HDL concentrations. It can be concluded that the administration of MSG may be considered as one of the main causes of obesity by increasing of leptin and insulin resistance and so developing of hyperphagia. Also it is accompanied by increasing the risk of atherosclerosis through development of diabetes mellitus type II and increasing total cholesterol and LDL. Moreover, maternal obesity is a serious condition that significantly impacts health of mothers and their children

Role of ghrelin in normotensive and hypertensive pregnant women

Ghrelin, an endogenous ligand for the growth hormone secretagogues, was originally isolated from rat stomach. Ghrelin exhibits a wide variety of actions including vasodilatation, increasing appetite, interaction with hypothalamic nuclei stimulating feeding and determining body weight gain, blocking leptininduced feeding reduction implying that there is a competitive interaction between ghrelin and leptin and increasing gastrointestinal motility. To clarify the haemodynamic and metabolic role of ghrelin in normotensive pregnant female, pregnancy induced hypertension, spontaneously hypertensive pregnant femaleand preclampsia. 120 pregnant womenwere divided into 4 groups [normal, pregnancy-associated hypertension, pregnancy-induced hypertension and preclampsia], each group included 30 pregnant women. Pregnant women, at 20-26 weeks, 26-32 weeks and after 32 weeks, were subjected to thorough history taking, clinical examination and laboratory investigations as blood picture, urine analysis, liver function tests and measurement of serum ghrelin, eptin, nitric oxide, lipid profile, insulin and glucose. Glomerular filtration rate [GFR], body mass index [BMI] and pregnancy outcome were also determined. Arterial blood pressure [ABP] [systolic blood pressure and diastolic blood pressure], ghrelin, leptin and cholesterol were increased while nitric oxide was decreased in pregnancy associated hypertension, pregnancy-induced hypertension [PIH] and preclampsia relative to normal pregnancy. Red blood cells [ABCs], platelets, GFR, HDL were decreased whereas SGOT, SGPT, fasting glucose, proteinuria and BMI were increased in preclampsia relative to other groups. Serum triglycerides and LDL were increased in pregnancy associated hypertension, preclampsia relative to normal pregnancy and PH. However, serum insulin was non significantly changed in all groups. Elevated ghrelin level, in pregnant women suffering from pre-existing chronic hypertension, PIH and preclampsia seems to play an important role in insulin level regulation, energy balance and bodyweight homeostasis, as well as control of cardiac and hemoclynamic functions

Effects of the Nitric oxide donor L-argjnine on the early stages of liver damage in rats treated with CCL[4]

This study aimed to evaluate the effects of nitric oxide [NO] donor L-arginine and consequently the NO on the early of liver damage and biochemical changes in rats Injected with CCL[4], Thirty two male albino rats weighing 180-220 g studied and divided into four groups. Group 1 rats were not injected or treated with any drug [control, n = 8]. Group 2 rats were injected with CCL[4] for 6 weeks [CCL[4] treated, n = 8]. Group 3 rats were injected with CCL[4] and L- arginine for 6 weeks [CCL[4]/L-argioina treated, n = 8]. Group 4 rats were injected with L-arginine and L-NAME intraperitoneal for 6 weeks [CCL[4]/L-arginine and L-NAME treated]. After 2 weeks of study, blood samples were collected for determination of activities of Alanine-transferase [ALT], aspartate amino-transferase [AST], alkaline phosphatase [AP] and the concentrations of total bilirubin. At the end of study the right lobe of liver was removed and divided into 2 pieces. The first piece used for histopathological examination by light microscopy and the second piece used for determination of NO concentration in tissue, The serum bilirubin and liver enzymes significantly increased in CCL[4] treated, and CCL[4]-L arginine and L-NANE treated groups in comparison with the control group, However, the liver enzymes were significantly in CCL[4]/L-arginine treated group in comparison with CCL[4] treated and CCL[4]/L-arginine and L-NAME treated groups. In the CCL[4] treated and CCL[4]/L-arginine and L-NAME treated groups the total nitrite [NOx] concentrations were significantly lower than in CCL[4]/untreated and CCL[4]/L-arginine treated groups. Histological Activity index Scores of the CCL[4]treated and CCL[4]/L-arginine and L-NAME treated groups were higher than in control group and CCL[4]/L-arginine treated groups. The degree of necro-inflammation and fibrosis showed significant difference between the CCL[4] and CCL[4]/L-arginine treated groups. In conclusion, the NO donor, L-arginine improved hepatic cell damage and fibrosis and positively affect serum amino transferase, alanine aminotransferase, and alkaline phosphatase mostly through increasing the concentrations of NOx in hepatic tissue