REVISITING THE ACUTE KIDNEY INJURY IN WISTAR RATS EXPERIMENTALLY ENVENOMATED WITY Bothrops jararacussu VENOM.

Toxicon ◽  
2021 ◽  
Author(s):  
Mayara A. Romanelli ◽  
Paula A. Soeiro ◽  
Raquel Costa da Silva ◽  
Rosilane Taveira-da-Silva ◽  
Paulo A. Melo ◽  
...  
2021 ◽  
Vol 22 (3) ◽  
pp. 1382
Author(s):  
Jelena Nesovic Ostojic ◽  
Milan Ivanov ◽  
Nevena Mihailovic-Stanojevic ◽  
Danijela Karanovic ◽  
Sanjin Kovacevic ◽  
...  

Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.


Author(s):  
Razvan Andrei CODEA ◽  
Mircea MIRCEAN ◽  
Sidonia Alina BOGDAN ◽  
Andras Laszlo NAGY ◽  
Alexandra BIRIS ◽  
...  

The identification of a suitable prevention method which facilitates limiting the deleterious effects of acute kidney injuries is highly required. In order to identify a proper treatment for acute kidney injuries, a suitable experimental model that replicates the structural, metabolic and inflammatory lesions that occur in the natural acute injured kidney is highly necessary. Intense urinary NAG activity can be found in a variety of renal disease such as toxic nephropathies, ischemic renal injury following cardiac surgery or renal transplantation but also in glomerular disease especially in diabetic nephropathy. Rises in urinary NAG enzyme activity strongly suggests tubular cell damage and support NAG enzyme as a biomarker of renal tubular injury. The aim of this paper is to obtain a stable in vivo acute kidney injury experimental model, in Wistar, rats and to evaluate the urinary activity of N-acetyl-β-D-glucosaminidase (NAG) enzyme, blood levels of urea and creatinine and microstructural renal alterations induced by ischemia/reperfusion injury respectively gentamicin nephrotoxicity. For this purpose we have used a rat experimental model. Adult male Wistar rats weighing 250-300 g were randomly divided into 3 groups with 8 rats in each group. Group 1 served as a model for the renal ischemia/reperfusion injury experiment, group 2 served for toxic kidney injury experimental model and group 3 served as control group. All individuals in both groups 1 and 2 presented marked elevations in blood urea and creatinine at the moment of euthanasia (day 3 for group 1 and day 9 for group 2) compared to the control group where biochemical values remained within normal limits. Urine analysis of both group 1 and 2 showed marked urinary NAG index activity which suggests acute tubular injury, suggestion confirmed by histological evaluation of the renal parenchyma sampled from this subjects


2014 ◽  
Vol 48 (5) ◽  
pp. 820-826 ◽  
Author(s):  
Franciele do Nascimento Santos ◽  
Mirian Watanabe ◽  
Carolina Ferreira Vasco ◽  
Cassiane Dezoti da Fonseca ◽  
Maria de Fatima Fernandes Vattimo

Objective Evaluating the effect of preconditioning with simvastatin in acute kidney injury induced by sepsis. Method Male adult Wistar rats were divided into the following groups: SHAM (control); SHAM+Statin (0.5 mg/kg simvastatin, orally); Sepsis (cecal puncture ligation – CPL); Sepsis+Statin. Physiological parameters, peritoneal fluid culture, renal function, oxidative metabolites, severity of acute kidney injury and animal survival were evaluated. Results The treatment with simvastatin in induced sepsis showed elevation of creatinine clearance with attenuation of generation of oxidative metabolites, lower severity of acute kidney injury and reduced mortality. Conclusion This investigation confirmed the renoprotection with antioxidant principle of the simvastatin in acute kidney injury induced by sepsis in an experimental model.


2020 ◽  
Vol 245 (16) ◽  
pp. 1474-1489
Author(s):  
Chandrashekar Annamalai ◽  
Rajesh N Ganesh ◽  
Pragasam Viswanathan

Acute kidney injury causes significant morbidity and mortality. This experimental animal study investigated the simultaneous impact of iron and vitamin D on acute kidney injury induced by iohexol, an iodinated, non-ionic monomeric radiocontrast agent in Wistar rats. Out of 36 healthy male Wistar rats, saline was injected into six control rats (group 1) and iohexol into the remaining 30 experimental rats (groups 2 to 6 comprising six rats each). Biochemical, renal histological changes, and gene expression of iron-regulating proteins and 1 α-hydroxylase were analyzed. Urinary neutrophil gelatinase-associated lipocalin (NGAL), serum creatinine, urine protein, serum and urine catalytic iron, 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and tissue lipid peroxidation were assayed. Rats injected with iohexol showed elevated urinary NGAL (11.94 ± 6.79 ng/mL), serum creatinine (2.92 ± 0.91 mg/dL), and urinary protein levels (11.03 ± 9.68 mg/mg creatinine) together with histological evidence of tubular injury and iron accumulation. Gene expression of iron-regulating proteins and 1 α-hydroxylase was altered. Serum and urine catalytic iron levels were elevated (0.57 ± 0.17; 48.95 ± 29.13 µmol/L) compared to controls (0.49 ± 0.04; 20.7 ± 2.62 µmol/L, P < 0.001). Urine catalytic iron positively correlated with tissue peroxidation (r = 0.469, CI 0.122 to 0.667, P = 0.004) and urinary NGAL (r = 0.788, CI 0.620 to 0.887, P < 0.001). 25-hydroxyvitamin D3 (61.58 ± 9.60 ng/mL) and 1,25-dihydroxyvitamin D3 (50.44 ± 19.76 pg/mL) levels increased simultaneously. In a multivariate linear regression analysis, serum iron, urine catalytic iron, and tissue lipid peroxidation independently and positively predicted urinary NGAL, an acute kidney injury biomarker. This study highlights the nephrotoxic potential of catalytic iron besides demonstrating a concurrent induction of vitamin D endogenously for possible renoprotection in acute kidney injury. Impact statement This work provides in-depth insights on catalytic iron-induced cytotoxicity and the resultant triggering of endogenous vitamin D synthesis in experimental acute kidney injury. Our results reveal significantly elevated levels of catalytic iron culminating in oxidant-mediated renal injury and a concomitant increase in 1,25-dihdyroxyvitamin D3 levels. Also, changes in other iron-related proteins including transferrin, ferritin, and hepcidin were observed both in the serum as well as in their mRNA expression. We consider all these findings vital since no connection between catalytic iron and vitamin D has been established so far. Furthermore, we believe that this work provides new and interesting results, with catalytic iron emerging as an important target in ameliorating renal cellular injury, possibly by timely administration of vitamin D. It also needs to be seen if these observations made in rats could be translated to humans by means of robust clinical trials.


2020 ◽  
Vol 9 (4) ◽  
pp. 249-255
Author(s):  
Dr.Kumayl Abbas Meghji ◽  
Dr.Tariq Feroz Memon ◽  
Dr. Imtiaz Ahmed ◽  
Dr. Sehar Gul Memon ◽  
Dr. Naila Noor ◽  
...  

Objective To evaluate the protective role of L-Arginine in cisplatin induced acute renal injury through assessment of renal, oxidative stress and inflammatory markers in albino wistar rats. Methods: Quasi-experimental study was conducted at the department of physiology and postgraduate research laboratory at Isra University, Hyderabad, Sindh from April 2019 to September 2019. Thirty male Albino wistar rats were selected through non-random purposive sampling and divided equally into three different groups: Group-A (Control group), Group-B (experimental group) received Cisplatin alone and Group-C (experimental group) received Cisplatin along with arginine. After sacrificing the animals, blood samples were collected through cardiac puncture while renal histopathological analysis was under the light microscope. The changes in severity were observed using a graded scale. Data was analysed using SPSS v23.0. Results: There was a statistically significant (p-value <0.05) decline in the bodyweight and rise in absolute kidney weight of group B in comparison with other two group. Moreover, significant rise (p-value <0.05) in serum renal markers was observed in group B while significant decline (p-value <0.05)  in these serum renal markers in group C compared with group B.  Furthermore, prominent demage in normal renal histology in group B rats while restoration of renal histology was demonstrated in group C rats. Conclusion: The present study concludes that L-Arginine exerts an anti-oxidative, anti-inflammatory and nephro-protective effect for renal tissue damage caused by Cisplatin. Keywords: Acute Kidney Injury, Antioxidant, Cisplatin, L-Arginine, Oxidative stress


2021 ◽  
pp. 1-11
Author(s):  
Adedeji David Atere ◽  
Olumide Faith Ajani ◽  
Akinpelu Moronkeji ◽  
Victory Oluwaseun Ajibade ◽  
Humphrey Benedo Osadolor

BACKGROUND: Insecticide usage has increased in the tropics and subtropics due to the high prevalence of vector-borne infections, even though insecticide use effectively reduces insect-borne diseases. Insecticide exposure can cause oxidative stress and have severe consequences for human health. The study was then designed to evaluate oxidative stress and its effects on immunomodulatory and renal integrity among Wistar rats exposed to pyrethroids. METHODS: Eighty-four Wistar rats were randomly selected and divided into two groups. Fifty-one rats were exposed to 1.2 %w/v pyrethroids, while the remaining thirty-three rats were grouped as non-exposed. The groups were divided into three different groups, each with 7, 21, and 41 days. After days of exposure, the animals in each group were anesthetized, and blood samples were collected from the inferior vena cava. Using standard spectrophotometric techniques, the levels of total antioxidant status (TAS), malondialdehyde (MDA), glutathione (GSH), hydrogen peroxide (H2O2), urea, creatinine and uric acid were determined. Blood activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) were determined. ELISA was used to determine levels of IgG, IgA, IgE, TNF-α, and NGAL. Data obtained were statistically compared. RESULTS: The serum mean levels of SOD, GPx, CAT, GSH, and TAS were significantly reduced (p <  0.05) while mean levels of MDA, H2O2, IgG, IgE, IgA, TNFα, neutrophil gelatinase-associated lipocalin (NGAL), urea, uric acid, and creatinine were significantly elevated (p <  0.05) from 7 to 41 days exposure in exposed groups. NGAL had a higher area under the ROC curve than urea and creatinine. CONCLUSIONS: This study observed that pyrethroids can cause oxidative stress, deplete antioxidant levels, nephrotoxicity, and may modulate both humoral and cellular immune functions. It also established NGAL as a sensitive diagnostic tool and early biomarker for acute kidney injury (AKI).


2019 ◽  
Vol 3 (4) ◽  
pp. 29-38
Author(s):  
Evi Lusiana ◽  
Nia Savitri Tamzil ◽  
Desi Oktarina

Background Kidney vital function as a regulator of blood volume and chemical composition to excrete solute and water selectively. Acute kidney injury (AKI) is a sudden decline in kidney function which is temporary, is marked by an increase in serum creatinine levels and decreased urine output. Objective This study aims to determine the effectiveness of cinnamon extract in acute kidney injury induced male wistar rats. Method An experimental in vivo with pre-post control group design was conducted in twenty-five wistar strain white rats that were divided into 5 treatment groups that received methylprednisolone as a positive control, aquades, and different dose of cinnamon extracts (50 mg/kgBW, 100 mg/kgBW, and 200 mg/kgBW). The rat model of acute kidney injury was prepared by the method of unilateral ureteral obstruction (UUO). The effectiveness of cinnamon extract was carried out by creatinine levels checked using ELISA and analyzed by ANOVA. Results The extract of cinnamon can lower serum creatinine levels were significantly (p <0.05). A dose of 100mg / KgBW is an effective dose in AKI compare to methylprednisolone. Conclusion Extract of cinnamon (Cinnamomum burmannii) corrected creatinine levels of acute kidney injury induced male wistar rats.   Keywords: Acute kidney injury, cinnamon extract, creatinine    


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