scholarly journals Impact of Chronic Cadmium Exposure on the Nephrotoxicity Sensitivity of Streptozotocin-Induced Diabetic Rats

2020 ◽  
Vol 7 (12) ◽  
pp. 5174-5178
Author(s):  
N’Guessan Assue Adja Julien ◽  
Adon Mousan Arsène ◽  
Kouassi Martin KONAN ◽  
Djaman Allico Joseph ◽  
Dosso Mireille
Keyword(s):  
Diabetic Nephropathy ◽  
Biochemical Parameters ◽  
Histopathological Examination ◽  
Inorganic Ions ◽  
Diabetic Rats ◽  
Cadmium Exposure ◽  
Renal Tubules ◽  
Tissue Samples ◽  
Cadmium Poisoning

The present study aimed to assess the role of subchronic cadmium exposure in the development of diabetic nephropathy. Diabetic rats induced by streptozotocin (STZ + Cd) and normal non-diabetic rats (Cd) were exposed to cadmium sulphate in drinking water at a dose of 200 mg / l for 30 days. After 30 days of cadmium poisoning, blood and tissue samples were taken to determine markers of kidney function (urea, uric acid, creatinine, total protein and inorganic ions) and for the achievement histological couples. Cadmium poisoning resulted in an increase in relative kidney weights and a change in biochemical parameters in serum. Histopathological examination of the kidneys revealed degeneration and necrosis of the renal tubules and shrinking of the glomeruli in rats poisoned with Cd. However, our results showed that diabetic rats induced by streptozotocin are more sensitive to nephrotoxicity of cadmium than rats normal. our results suggest that cadmium may be a factor in the development of diabetic nephropathy.

scholarly journals The role of nicotinamide in the correction of renal function in diabetic nephropathy

2019 ◽  
Vol 23 (2) ◽  
pp. 218-221
Author(s):  
L. V. Yanitskaya ◽  
L. F. Osinskaya ◽  
A. V. Redko
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Diabetic Nephropathy ◽  
Statistical Analysis ◽  
Rat Kidney ◽  
Clinical Manifestations ◽  
Diabetic Rats ◽  
Cortical Layer ◽  
The Difference

Hyperglycemia of diabetes mellitus leads to the activation of the polyol way of oxidation of glucose with the activation of the enzymes of aldose reductase and sorbitol dehydrogenase and of their coenzymes NADPH and NAD, which triggers the mechanism of formation of sorbitol. The consequences of these changes lead to microangiopathy of the tissues of the kidneys, which may be one of the pathogenetic mechanisms of diabetic nephropathy. In an accessible literature, the role of coenzymes of sorbitol pathway in the development of diabetic nephropathy is not sufficiently defined. The purpose of the study was to study the content of NAD and NADPH coenzymes, their correlation, and their role in the mechanism of kidney damage in diabetes mellitus and to predict the possible correction of these changes with the NAD-nicotinamide derivative. The study was conducted on a model of streptotrozectinic diabetes mellitus (single administration of streptozotocin in a dose of 60 mg per 1 kg of body weight). Four weeks after induction of diabetes, nicotinamide (100 mg per 1 kg body weight) was injected. The level of glucose was determined by the Accu-chek (Roshe Diagnostics, Switzerland) glucose meter. The content of NAD and NADH was determined in the non-protein extracts. The statistical analysis was carried out using the Microsoft Excel statistical analysis program. The difference between the indicators was considered statistically significant (p<0.05). The NAD level was reduced by 31%, the NAD/NADN ratio was 32%. The dependence of the ratio of NADP/NADPN in conditions of hyperglycemia of diabetes mellitus with clinical manifestations of diabetic nephropathy is determined. A decrease in the ratio of NADP/NADPN to 38% in the rat kidney in the cortical layer was detected. The introduction of nicotinamide normalized the reduced content of NAD diabetic rats. These results provide perspectives for further research in which nicotinamide can be used as a renal protector.

Sildenafil, a phosphodiesterase type 5 inhibitor, attenuates diabetic nephropathy in STZ-induced diabetic rats

2016 ◽  
Vol 27 (1) ◽  
Author(s):  
Alok Shiomurti Tripathi ◽  
Papiya Mitra Mazumder ◽  
Anil Vilasrao Chandewar
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Diabetic Nephropathy ◽  
Triglyceride Level ◽  
Biochemical Parameters ◽  
Treated Group ◽  
Diabetic Rats ◽  
Treatment Results ◽  
Phosphodiesterase Type 5 Inhibitor ◽  
Phosphodiesterase Type

AbstractThe present study evaluates the possible mechanism of sildenafil citrate (SIL) for the attenuation of renal failure in diabetic nephropathic (DN) animals.Diabetic nephropathy was induced by a single dose of streptozotocin (STZ) (60 mg/kg, i.p.) and confirmed by assessing the blood and urine biochemical parameters on the 28th day of its induction. The selected DN animals were treated with glimepiride (0.5 mg/kg, p.o.) and SIL (2.5 mg/kg, p.o.) for a period of 6 weeks. Biochemical parameters in blood and urine were estimated after the 29th and 70th day of the protocol for the estimation of the effect of SIL.There were significant alterations in the blood and urine biochemical parameters in STZ-treated groups which confirmed DN. There was a significant decrease in the triglyceride level in the SIL-only-treated group on the 70th day of the protocol. The histopathology study also suggested that SIL treatment results in the improvement in the podocyte count in DN animals.The present study concludes that SIL improves the renal function by decreasing the triglyceride level and improving the podocyte count in DN animals.

scholarly journals Alteration of urinary sorbitol excretion in WBN-kob diabetic rats - treatment with an aldose reductase inhibitor

2004 ◽  
Vol 181 (3) ◽  
pp. 429-435 ◽  
Author(s):  
T Tsugawa ◽  
R Shinohara ◽  
A Nagasaka ◽  
I Nakano ◽  
F Takeda ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Aldose Reductase ◽  
Whole Blood ◽  
Reductase Inhibitor ◽  
Cell Function ◽  
Polyol Pathway ◽  
Diabetic Rats ◽  
Aldose Reductase Inhibitor ◽  
Tubular Damage ◽  
Renal Tubules

An accelerated polyol pathway in diabetes contributes to the development of diabetic complications. To elucidate diabetic nephropathy involving also renal tubular damage, we measured urinary sorbitol concentration concomitantly with urinary N-acetyl-D-glucosaminidase (NAG) excretion in WBN-kob diabetic rats.Twenty-four-hour urinary sorbitol concentrations increased in the diabetic rats in parallel with whole blood sorbitol concentrations. An increase in 24-h urinary NAG excretion coincided with the elevated urinary sorbitol levels in the diabetic rats. The administration of epalrestat, an aldose reductase inhibitor, reduced the increased whole blood and urinary sorbitol concentrations and urinary NAG excretion concomitantly with renal aldose reductase inhibition in the diabetic rats.These results indicate that diabetic nephropathy involves distorted cell function of renal tubules, and that treatment with epalrestat may prevent at least the progress of the nephropathy.

scholarly journals THE ROLE OF STEM CELL INJECTION IN AMELIORATION OF DIABETIC NEPHROPATHY IN EXPERIMENTALLY INDUCED DIABETIC RATS.

2016 ◽  
Vol 4 (10) ◽  
pp. 1412-1419
Author(s):  
MohammedSamy Fawzy ◽  
◽  
AmalFathy Gharib ◽  
SallyMahmoud Shalaby ◽  
HanimMagdy Abdel-Nour ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Stem Cell ◽  
Diabetic Rats ◽  
Cell Injection ◽  
Stem Cell Injection ◽  
Experimentally Induced

scholarly journals Apigenin ameliorates streptozotocin-induced diabetic nephropathy in rats via MAPK-NF-κB-TNF-α and TGF-β1-MAPK-fibronectin pathways

2017 ◽  
Vol 313 (2) ◽  
pp. F414-F422 ◽  
Author(s):  
Salma Malik ◽  
Kapil Suchal ◽  
Sana Irfan Khan ◽  
Jagriti Bhatia ◽  
Kamal Kishore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Transforming Growth Factor ◽  
Mapk Pathway ◽  
Histopathological Examination ◽  
Fasting Blood Glucose ◽  
Transforming Growth Factor Β1 ◽  
Diabetic Rats ◽  
Tnf Α ◽  
Per Se

Diabetic nephropathy (DN), a microvascular complication of diabetes, has emerged as an important health problem worldwide. There is strong evidence to suggest that oxidative stress, inflammation, and fibrosis play a pivotal role in the progression of DN. Apigenin has been shown to possess antioxidant, anti-inflammatory, antiapoptotic, antifibrotic, as well as antidiabetic properties. Hence, we evaluated whether apigenin halts the development and progression of DN in streptozotocin (STZ)-induced diabetic rats. Male albino Wistar rats were divided into control, diabetic control, and apigenin treatment groups (5–20 mg/kg po, respectively), apigenin per se (20 mg/kg po), and ramipril treatment group (2 mg/kg po). A single injection of STZ (55 mg/kg ip) was administered to all of the groups except control and per se groups to induce type 1 diabetes mellitus. Rats with fasting blood glucose >250 mg/dl were included in the study and randomized to different groups. Thereafter, the protocol was continued for 8 mo in all of the groups. Apigenin (20 mg/kg) treatment attenuated renal dysfunction, oxidative stress, and fibrosis (decreased transforming growth factor-β1, fibronectin, and type IV collagen) in the diabetic rats. It also significantly prevented MAPK activation, which inhibited inflammation (reduced TNF-α, IL-6, and NF-κB expression) and apoptosis (increased expression of Bcl-2 and decreased Bax and caspase-3). Furthermore, histopathological examination demonstrated reduced inflammation, collagen deposition, and glomerulosclerosis in the renal tissue. In addition, all of these changes were comparable with those produced by ramipril. Hence, apigenin ameliorated renal damage due to DN by suppressing oxidative stress and fibrosis and by inhibiting MAPK pathway.

scholarly journals Clinicopathological Study of Cholecystectomy Specimens

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 2366-2370
Author(s):  
Sujata R Kanetkar ◽  
Anand Gudur ◽  
Rohit S Kadam ◽  
Atul B Hulwan ◽  
Pawar S J
Keyword(s):  
Odds Ratio ◽  
Biochemical Parameters ◽  
Blood Sugar Level ◽  
Clinical Presentation ◽  
Histopathological Examination ◽  
Chronic Cholecystitis ◽  
Diabetic Patients ◽  
Significant Odds Ratio ◽  
Treatment Prognosis

In this study, there are possible causes of two years from June 2015 to May of 2017. During study includes 130 cases of cholecystectomy specimens from January 2013 to June 2017. The objective/purpose of the study is to correlate histopathological findings with various biochemical parameters viz. fasting blood sugar level, lipid profile, etc. Amongst the four cases of adenocarcinoma, 3 (75 %) cases showed serosal infiltration and liver infiltration. Out of a total of 130 cases, 69 (53%) were female, and 61 (47%) were male. Out of 4 patients of adenocarcinoma 2 (50%) patients expired during the postoperative period, while 2 (50%) patients improved. Diabetic patients constitute 13.84% of total cholecystectomy patients, so diabetes proved to be a risk factor for the development of gallbladder diseases with statistically significant Odds Ratio (2.66). Results from this study show that a variety of gallbladder lesions are observed in cholecystectomy specimens. The most common lesion observed was chronic cholecystitis with cholelithiasis 99 cases (76.1%), followed by acute cholecystitis 12 cases (9.2%). The present study was undertaken to emphasize the role of histopathological examination in cholecystectomy specimens and its correlation with clinical presentation. Histopathological examination many time reveals an unusual diagnosis bearing significant implications on the treatment, prognosis and outcome of the patient. Hence, the study was undertaken to emphasize the role of histopathological examination in cholecystectomy specimens and its correlation with clinical presentation.

scholarly journals Protective effect of C-peptide on experimentally induced diabetic nephropathy and the possible link between C-peptide and nitric oxide

2018 ◽  
Vol 43 (6) ◽  
pp. 617-624 ◽  
Author(s):  
Eman A. Elbassuoni ◽  
Neven M. Aziz ◽  
Nashwa F. El-Tahawy
Keyword(s):  
Nitric Oxide ◽  
Diabetic Nephropathy ◽  
Diabetic Complications ◽  
Renal Tissue ◽  
Diabetic Rats ◽  
Necrosis Factor Alpha ◽  
C Peptide ◽  
Experimentally Induced

Diabetic nephropathy one of the major microvascular diabetic complications. Besides hyperglycemia, other factors contribute to the development of diabetic complications as the proinsulin connecting peptide, C-peptide. We described the role of C-peptide replacement therapy on experimentally induced diabetic nephropathy, and its potential mechanisms of action by studying the role of nitric oxide (NO) as a mediator of C-peptide effects by in vivo modulating its production by NG-nitro-l-arginine methyl ester (L-NAME). Renal injury markers measured were serum urea, creatinine, tumor necrosis factor alpha, and angiotensin II, and malondialdehyde, total antioxidant, Bcl-2, and NO in renal tissue. In conclusion, diabetic induction resulted in islet degenerations and decreased insulin secretion with its metabolic consequences and subsequent renal complications. C-Peptide deficiencies in diabetes might have contributed to the metabolic and renal error, since C-peptide treatment to the diabetic rats completely corrected these errors. The beneficial effects of C-peptide are partially antagonized by L-NAME coadministration, indicating that NO partially mediates C-peptide effects.

scholarly journals Anti-diabetic Effect of Acridocarpus Orientalis

2020 ◽  
Vol 14 (1) ◽  
pp. 132-144
Author(s):  
Mohamed Lotfy ◽  
Taoufik S. Ksiksi ◽  
Abdul Rasheed Palakkot ◽  
Crystal M. D’Souza ◽  
Sahar Mohsin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
New Caledonia ◽  
Islet Cells ◽  
Histopathological Examination ◽  
Serum Insulin ◽  
Antioxidant Properties ◽  
Pancreatic Tissue ◽  
Diabetic Rats ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tissue Samples

Background: Acridocarpus orientalis (AO) is a medicinal herb indigenous to tropical and subtropical Africa, Arabian Peninsula, and New Caledonia with reported anti-inflammatory and antioxidant properties. Objective: To determine whether AO has any beneficial effects on diabetes-induced metabolic parameters in rats. Materials and Methods: Diabetes mellitus was induced in male Wistar rats by streptozotocin. Diabetic rats were treated with three doses of AO extract (50, 100, and 200 mg/kg BW) for 30 days. Kidney, liver, and pancreatic tissue samples were processed for histopathology to determine the effect of AO on the cells of these organs. The effect of AO on pancreatic islet cells and serum insulin levels was also examined using immunohistochemistry and enzyme-linked immunosorbent assay techniques, respectively. Results: AO (100 mg/kg BW) caused a marked reduction in blood glucose levels in diabetic rats compared to diabetic control on day 10 of the study. Moreover, AO (200 mg/kg BW) increased the number of insulin-positive cells with a concomitant reduction in the number of glucagon-immunoreactive cells in pancreatic islets. AO (100 mg/kg) also increased the serum level of superoxide dismutase significantly. Although the administration of AO was able to significantly decrease the diabetes-associated increases in serum creatinine and bilirubin levels, it had no effect on blood urea nitrogen, serum aspartate, or alanine aminotransferase levels. Histopathological examination showed that AO has no toxic effect on the structure of the pancreas, liver, and kidney. Conclusion: Our findings showed that AO could alleviate some complications of diabetes mellitus.

scholarly journals Effect of Cadmium Exposure on Zinc Levels in Normal Non-Diabetic and Diabetic Rats Induced by Streptozotocin

2020 ◽  
Vol 8 (8) ◽  
pp. 507-512
Author(s):  
N’ Guessan Assue Adja Julien ◽  
Adon Mousan Arsène ◽  
Konan Kouassi Martin ◽  
Djaman Allico Joseph ◽  
Dosso Mireille
Keyword(s):  
Drinking Water ◽  
Diabetic Rats ◽  
Cadmium Exposure ◽  
Toxic Effects ◽  
Control Group ◽  
Cadmium Poisoning ◽  
Zinc Levels ◽  
Cadmium Zinc

Diabetic rats induced by streptozotocin and normal non-diabetic rats were exposed to cadmiumsulphate in drinking water at a dose of 200 mg / L for 30 days. At the end of the exposure, theblood, kidney and pancreas of each rat were taken for the determination of cadmium and zinc.The results show a significant increase in the level of cadmium in the blood, kidney andpancreas of normal non-diabetic rats and diabetic rats compared to the control group. Thecadmium concentration was significantly higher in plasma and tissues in diabetic rats comparedto normal non-diabetic rats. Cadmium poisoning resulted in a significant decrease in the levelof zinc in the blood and tissues of normal non-diabetic rats and diabetic rats compared to theirrespective controls. This study reveals that diabetic rats induced by streptozotocin are moresensitive to the toxic effects of cadmium than normal rats.Key words: Cadmium, zinc, plasma, pancreas, kidneys, diabetes

scholarly journals Aminoguanidine Ameliorates Overexpression of Prosclerotic Growth Factors and Collagen Deposition in Experimental Diabetic Nephropathy

2001 ◽  
Vol 12 (10) ◽  
pp. 2098-2107 ◽  
Author(s):  
DARREN J. KELLY ◽  
RICHARD E. GILBERT ◽  
ALISON J. COX ◽  
TINA SOULIS ◽  
GEORGE JERUMS ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Growth Factors ◽  
Growth Factor ◽  
Experimental Diabetes ◽  
Fold Increase ◽  
Diabetic Rats ◽  
Renal Tubules ◽  
Collagen Deposition ◽  
Matrix Deposition ◽  
Tgf Β1

Abstract. Profibrotic cytokines and the formation of advanced-glycation end products (AGE) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. However, tubulointerstitial pathology is also an important determinant of progressive renal dysfunction in diabetic nephropathy. This study sought to investigate the expression of profibrotic growth factors and matrix deposition in the glomerulus and the tubulointerstitium and to examine the effect of blocking AGE formation in experimental diabetic nephropathy. Thirty-six male Sprague-Dawley rats were randomized into control and diabetic groups. Diabetes was induced in 24 rats by streptozotocin. Twelve diabetic rats were further randomized to receive the inhibitor of AGE formation, aminoguanidine (1 g/l drinking water). At 6 mo, experimental diabetes was associated with a three-fold increase in expression of transforming growth factor (TGF)-β1 (P< 0.01versuscontrol) and five-fold increase in platelet-derived growth factor (PDGF)-B gene expression (P< 0.01versuscontrol) in the tubulointerstitium.In situhybridization demonstrated a diffuse increase in both TGF-β1 and PDGF-B mRNA in renal tubules. Aminoguanidine attenuated not only the overexpression of TGF-β1 and PDGF-B but also reduced type IV collagen deposition in diabetic rats (P< 0.05). TGF-β1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. The observed beneficial effects of aminoguanidine on the tubulointerstitium in experimental diabetes suggest that AGE-mediated expression of profibrotic cytokines may contribute to tubulointerstitial injury and the pathogenesis of diabetic nephropathy.

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