scholarly journals Olmesartan Attenuates Tacrolimus-Induced Biochemical and Ultrastructural Changes in Rat Kidney Tissue

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Naif O. Al-Harbi ◽  
Faisal Imam ◽  
Mohammed M. Al-Harbi ◽  
Muzaffar Iqbal ◽  
Ahmed Nadeem ◽  
...  
Keyword(s):  
Renal Damage ◽  
Calcineurin Inhibitor ◽  
Renal Tubule ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Immunosuppressive Agent ◽  
Ultrastructural Changes ◽  
Protective Effects ◽  
Ultrastructural Studies ◽  
Induced Changes

Tacrolimus, a calcineurin inhibitor, is clinically used as an immunosuppressive agent in organ transplantation, but its use is limited due to its marked nephrotoxicity. The present study investigated the effect of olmesartan (angiotensin receptor blocker) on tacrolimus-induced nephrotoxicity in rats. A total of 24 rats were divided into four groups, which included control, tacrolimus, tacrolimus + olmesartan, and olmesartan groups. Tacrolimus-induced nephrotoxicity was assessed biochemically and histopathologically. Tacrolimus significantly increased BUN and creatinine level. Treatment with olmesartan reversed tacrolimus-induced changes in the biochemical markers (BUN and creatinine) of nephrotoxicity. Tacrolimus significantly decreased GSH level and catalase activity while increasing MDA level. Olmesartan also attenuated the effects of tacrolimus on MDA, GSH, and catalase. In tacrolimus group histological examination showed marked changes in renal tubule, mitochondria, and podocyte processes. Histopathological and ultrastructural studies showed that treatment with olmesartan prevented tacrolimus-induced renal damage. These results suggest that olmesartan has protective effects on tacrolimus-induced nephrotoxicity, implying that RAS might be playing role in tacrolimus-induced nephrotoxicity.

scholarly journals Effect of Trigonella Foenum against Ethylene Diamine Tetra Acetic Acid induced Nephrotoxicity in Male Albino Rats

2020 ◽  
Vol 1 (1) ◽  
pp. 32-43
Author(s):  
A I Barakat ◽  
EH Radwan
Keyword(s):  
Creatinine Clearance ◽  
Aqueous Extract ◽  
Renal Damage ◽  
Kidney Tissue ◽  
Free Radical Scavenger ◽  
Albino Rats ◽  
Radical Scavenger ◽  
Protective Agent ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers

Background Nephrotoxicity is a complication due to the effect of some toxic chemicals on kidney. Current study planned to screen the effect of Trigonella foenumaqueous seeds extracts on EDTA induced nephrotoxicity. Trigonella foenum known for its various medicinal properties is also a natural antioxidant and a free radical scavenger with no documented evidence as a nephron-protective agent. Objective To investigate the protective effects of aqueous seed extracts of Trigonella foenum. Material and Methods The present study was used 40 male albino rats (Rattus albinus) with weight of (150 ± 10) g with divided into four groups: control gp; EDTA gp (95 mg/kg); Trigonella foenum gp (500 mg/kg) and EDTA + Trigonella f oenum gp by gastric tube daily for 4 weeks. Blood urea, creatinine, GFR, creatinine clearance, MDA and GPx analyses and microscopic examination of kidney were performed. Results In the present study, Blood samples were taken from all groups and concentration of serum urea, creatinine, GFR, Creatinine clearance, MDA and GPx were determined. Histopathological observations were observed in kidney tissue. Data were analyzed using analysis of variance (ANOVA). EDTA induced an increase in urea and creatinine as well as there was a decrease in the concentration of GFR and creatinine clearance. The level of MDA was increase while the concentration of GPx was decrease in the serum of EDTA group. The aqueous extracts of Trigonella seeds significantly prevented renal damage by normalizing increased levels of renal markers. The correction of oxidative stress biomarkers was consistent with amelioration of the histopathological changes induced by EDTA. Hence, it is suggested that ameliorative effect of aqueous extract of Trigonella foenumagainst EDTA induced nephrotoxicity. Conclusion The present data suggest that aqueous extract of Trigonella foenum exhibits reno-protective effect in EDTA induced renal damage.

scholarly journals Protective effect of ganoderan on renal damage in rats with chronic glomerulonephritis

2008 ◽  
Vol 31 (4) ◽  
pp. 212 ◽  
Author(s):  
Wei-De Zhong ◽  
Hui-Chan He ◽  
Ru-Biao Ou ◽  
Xue-Cheng Bi ◽  
Qi-Shan Dai ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Protective Effect ◽  
Renal Damage ◽  
Light And Electron Microscopy ◽  
Kidney Tissue ◽  
Chronic Glomerulonephritis ◽  
Protective Effects ◽  
Model Group ◽  
Sprague Dawley ◽  
Urine Protein

Purpose: To investigate the protective effect of ganoderan on renal damage in rat models with chronic glomerulonephritis induced by adriamycin. Methods: 48 healthy Sprague-Dawley rats were randomly divided into three groups: control, nephritic model and ganoderan treatment groups. Changes of the following indices in the three groups were observed 6 weeks after treatment: 24-hour urine protein, albumen, serum creatinine, cholesterol. Histopathological observations of the renal cortex were made by light and electron microscopy. Results: Compared with controls, levels of 24-hour urine protein (9.60±0.57mg/d vs. 82.50±3.18mg/d), serum creatinine (35.25±2.63?mol/L vs. 44.75±8.06?mol/L) and cholesterol (1.15±0.10mmol/L vs. 4.02±0.25mmol/L) of rats in the nephritic model group were increased (P < 0.05), and the concentration of albumen was decreased (35.98±1.34g/L vs. 19.05±0.62g/L, P < 0.05). Ganoderan administration decreased 24-hour urine protein (82.50±3.18mg/d vs. 45.01±3.94mg/d, P < 0.05). Following ganoderan, the pathological changes in kidney tissue were improved compared with those in the nephritic model group. Conclusion: Ganoderan exerts protective effects in rats with chronic glomerulonephritis induced by ADR. Ganoderan reduced 24-hour urine protein, serum creatinine, cholesterol, improving renal function and reducing the severity of renal injury.

Ultrastructural changes in the rat kidney after single dose of cyclophosphamide—Possible roles for peroxisome proliferation and lysosomal dysfunction in cyclophosphamide-induced renal damage

2011 ◽  
Vol 30 (12) ◽  
pp. 1924-1930 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac
Keyword(s):  
Electron Microscopy ◽  
Single Dose ◽  
Renal Damage ◽  
Rat Kidney ◽  
Ultrastructural Changes ◽  
Peroxisome Proliferation ◽  
Time Intervals ◽  
Subcellular Organelles ◽  
Renal Tubular Cells ◽  
Renal Tubular

Electron microscopy was used to examine changes in the subcellular organelles of the rat kidney at different time intervals after a single exposure to cyclophosphamide (CP). The morphological changes were studied at different time points (6 hrs, 16 hrs and 24 hrs) after a single-dose administration of CP. Six rats were killed at each time intervals after the administration of CP. Saline-treated rats served as controls. CP administration resulted in alterations in various subcellular organelles including peroxisomes, lysosomes, mitochondria, and the endoplasmic reticulum (ER) of the renal tubular epithelium as well as damage to the glomerulus. The basement membrane of the glomerulus was thickened. Many podocytes were destroyed. The nucleoplasm of the endothelial cell showed fewer granularities. The tubules were distorted and the brush border was destroyed. Two striking features in the renal tubular cells are increase in number and size of the peroxisomes (peroxisome proliferation) and decrease in the number of lysosomes. The mitochondria were elongated and the number was increased in the tubules of CP-treated rats. The ER was dilated. Cell necrosis was also seen. This study is an evidence of changes in morphology of rat kidney after induction of renal damage by a single dose of CP. Since transmission electron microscopy is the highest magnification tool at present, it can be useful in estimating the degree of injury and outcome of alternative treatment strategies in the management of CP-induced renal damage after establishing a scoring system.

Ultrastructural studies of the effect of cystamine on primary rat proximal tubular cell (PTC) cultures

1987 ◽  
Vol 45 ◽  
pp. 874-875
Author(s):  
K. Koizumi ◽  
T. Nishihira ◽  
K. A. Elliget ◽  
P. C. Phelps ◽  
I. K. Berezesky ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Primary Cultures ◽  
Isolated Hepatocytes ◽  
Ultrastructural Changes ◽  
Kidney Cortex ◽  
Isolated Perfused Rat Liver ◽  
Rat Kidney Cortex ◽  
Ultrastructural Studies ◽  
Phospholipid Hydrolysis ◽  
Intracellular Ca

Cystamine has been shown to alter intracellular Ca2+ homeostasis in isolated perfused rat liver and isolated hepatocytes by inhibiting Ca2+ efflux. This inhibition of the active extrusion of Ca2+ from hepatocytes is associated with the formation of mixed disulfides between cystamine and plasma membrane thiols and a subsequent inactivation of Ca2+-ATPase. The resulting sustained increase in cytosolic free Ca2+ is followed by both proteolysis and phospholipid hydrolysis, the proposed mechanism of hepatotoxicity.We have investigated cystamine-induced nephrotoxicity in PTC primary cultures. This study reports ultrastructural changes in kidney cells resulting from exposure to 10 mM cystamine for 15, 60, 120 and 180 min.Primary tubular cells were isolated from male Fischer 344 rat kidney cortex and maintained in a 50:50 mixture of DME and Ham's F12. Four day-old cultures were treated with cystamine, washed twice with HBSS, fixed in 4% phosphate-buffered formaldehyde:1% glutaraldehyde, post-fixed is OsO4, dehydrated through an ethanol series and embedded in Polybed 812. Ultrathin sections were examined in a JEOL 100B electron microscope.

Electron microscopic study of the membrane glycoproteins in the rat kidney after cisplatin treatment

1989 ◽  
Vol 47 ◽  
pp. 912-913
Author(s):  
S.K. Aggarwal
Keyword(s):  
Alkaline Phosphatase ◽  
Rat Kidney ◽  
Light And Electron Microscopy ◽  
Kidney Tissue ◽  
Membrane Glycoproteins ◽  
Electron Microscopic ◽  
Before And After ◽  
Interstrand Cross Links ◽  
Cross Links

The proposed primary mechanism of action of the anticancer drug cisplatin (Cis-DDP) is through its interaction with DNA, mostly through DNA intrastrand cross-links or DNA interstrand cross-links. DNA repair mechanisms can circumvent this arrest thus permitting replication and transcription to proceed. Various membrane transport enzymes have also been demonstrated to be effected by cisplatin. Glycoprotein alkaline phosphatase was looked at in the proximal tubule cells before and after cisplatin both in vivo and in vitro for its inactivation or its removal from the membrane using light and electron microscopy.Outbred male Swiss Webster (Crl: (WI) BR) rats weighing 150-250g were given ip injections of cisplatin (7mg/kg). Animals were killed on day 3 and day 5. Thick slices (20-50.um) of kidney tissue from treated and untreated animals were fixed in 1% buffered glutaraldehyde and 1% formaldehyde (0.05 M cacodylate buffer, pH 7.3) for 30 min at 4°C. Alkaline phosphatase activity and carbohydrates were demonstrated according to methods described earlier.

scholarly journals Quantitative Proteomic Analysis of Plasma after Remote Ischemic Conditioning in a Rhesus Monkey Ischemic Stroke Model

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1164
Author(s):  
Siying Song ◽  
Linlin Guo ◽  
Di Wu ◽  
Jingfei Shi ◽  
Yunxia Duan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Rhesus Monkey ◽  
Proteomic Analysis ◽  
Complement C3 ◽  
Protective Effects ◽  
Plasma Proteome ◽  
Remote Ischemic Conditioning ◽  
Ischemic Conditioning ◽  
Metabolism Regulation ◽  
Induced Changes

Background: Animal and clinical studies have shown that remote ischemic conditioning (RIC) has protective effects for cerebral vascular diseases, with induced humoral factor changes in the peripheral blood. However, many findings are heterogeneous, perhaps due to differences in the RIC intervention schemes, enrolled populations, and sample times. This study aimed to examine the RIC-induced changes in the plasma proteome using rhesus monkey models of strokes. Methods: Two adult rhesus monkeys with autologous blood clot-induced middle cerebral artery (MCA) occlusion underwent RIC interventions twice a week for five consecutive weeks. Each RIC treatment included five cycles of five minutes of ischemia alternating with five minutes of reperfusion of the forearm. The blood samples were taken from the median cubital vein of the monkeys at baseline and immediately after each week’s RIC stimulus. The plasma samples were isolated for a proteomic analysis using mass spectrometry (MS). Results: Several proteins related to lipid metabolism (Apolipoprotein A-II and Apolipoprotein C-II), coagulation (Fibrinogen alpha chain and serpin), immunoinflammatory responses (complement C3 and C1), and endovascular hemostasis (basement membrane-specific heparan sulfate proteoglycan) were significantly modulated after the RIC intervention. Many of these induced changes, such as in the lipid metabolism regulation and anticoagulation responses, starting as early as two weeks following the RIC intervention. The complementary activation and protection of the endovascular cells occurred more than three weeks postintervention. Conclusions: Multiple protective effects were induced by RIC and involved lipid metabolism regulation (anti-atherogenesis), anticoagulation (antithrombosis), complement activation, and endovascular homeostasis (anti-inflammation). In conclusion, this study indicates that RIC results in significant modulations of the plasma proteome. It also provides ideas for future research and screening targets.

scholarly journals Identification of vasopressin and determination of its corticomedullary levels in rat kidney tissue

1984 ◽  
Vol 26 (6) ◽  
pp. 785-790 ◽  
Author(s):  
Kurakazu Shimizu ◽  
Akihide Nakao ◽  
Tatsuya Nonaka ◽  
Hiroshi Oka
Keyword(s):  
Rat Kidney ◽  
Kidney Tissue

Does Crystal Deposition in Genetic Hypercalciuric Rat Kidney Tissue Share Similarities With Bone Formation?

Urology ◽  
2014 ◽  
Vol 83 (2) ◽  
pp. 509.e7-509.e14 ◽  
Author(s):  
Zhaohui Jia ◽  
Shaogang Wang ◽  
Jinhui Tang ◽  
Deng He ◽  
Lei Cui ◽  
...  
Keyword(s):  
Bone Formation ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Crystal Deposition

Inflammatory response and matrix metalloproteinases in chronic kidney failure: Modulation by adropin and spexin

2021 ◽  
pp. 153537022110124
Author(s):  
Burak Yazgan ◽  
Filiz Avcı ◽  
Gülsün Memi ◽  
Ebru Tastekin
Keyword(s):  
Inflammatory Response ◽  
Kidney Failure ◽  
Renal Damage ◽  
Urine Volume ◽  
Kidney Tissue ◽  
Public Health Problem ◽  
Chronic Kidney Failure ◽  
Urine Protein ◽  
Cox 2 ◽  
Cox 1

Chronic kidney disease is a major global public health problem. The peptide hormones adropin and spexin modulate many physiological functions such as energy balance and glucose, lipid and protein metabolism. However, it is unclear whether these peptides may exert effects on renal damage, tissue remodeling, and inflammatory conditions. In view of the limited information, we aimed to investigate the effect of adropin and spexin on matrix metalloproteinase and inflammatory response genes a rat model of adenine-induced chronic kidney failure. Chronic kidney failure was induced in rats by administering adenine hemisulfate. Renal function was determined in an autoanalyzer. Histopathological modifications were assessed by H&E staining. mRNA expression levels of ALOX 15, COX 1, COX 2, IL-1β, IL-10, IL-17A, IL-18 IL-21, IL-33, KIM-1, MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-13, NGAL, TGFβ1, TIMP-1, and TNFα in kidney tissue were measured by qPCR. Our results showed an increase of 24-h urine volume, serum creatinine, BUN, and urine protein levels in group with adenine-induced CKF. Adropin and spexin treatments decreased urine protein and 24-h urine volume. Renal damage, TIMP-1, IL-33, and MMP-2 increased after CKF induction, while COX 1, MMP-9, and MMP-13 levels were significantly reduced. Furthermore, KIM-1, TIMP-1, IL-33, and MMP-2 were downregulated by spexin treatment. Renal damage, NGAL, TIMP-1 IL-17A, IL-33, MMP-2, and MMP-3 decreased after adropin treatment, while MMP-13 levels were upregulated. Treatment with adropin+spexin decreased KIM-1, NGAL, TIMP-1, IL-1β, IL-17A, IL-18, IL-33, ALOX 15, COX 1, COX 2, TGFβ1, TNFα, MMP-2, MMP-3, and MMP-7, but increased MMP-13 levels. Our findings revealed that inflammatory response and MMP genes were modulated by adropin and spexin. These peptides may have protective effects on inflammation and chronic kidney damage progression.

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