scholarly journals The Effects of Vitamin D on Gentamicin-Induced Acute Kidney Injury in Experimental Rat Model

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ender Hur ◽  
Alev Garip ◽  
Asuman Camyar ◽  
Sibel Ilgun ◽  
Melih Ozisik ◽  
...  
Keyword(s):  
Vitamin D ◽  
Acute Kidney Injury ◽  
Rat Model ◽  
Urine Volume ◽  
Kidney Injury ◽  
Control Group ◽  
Albino Rats ◽  
Tubular Injury ◽  
Renal Histology ◽  
Experimental Rat Model

Introduction. Acute kidney injury (AKI) pathogenesis is complex. Findings of gentamicin nephrotoxicity are seen in 30% of the AKI patients. Vitamin D has proven to be effective on renin expression, inflammatory response, oxidative stress, apoptosis, and atherosclerosis. We aimed to investigate the effect of vitamin D in an experimental rat model of gentamicin-induced AKI.Methods. Thirty nonuremic Wistar albino rats were divided into 3 groups: Control group, 1 mL saline intramuscular (im) daily; Genta group, gentamicin 100 mg/kg/day (im); Genta + vitamin D, gentamicin 100 mg/kg/day (im) in addition to 1α, 25 (OH)2D30.4 mcg/kg/day subcutaneously for 8 days. Blood pressures and 24-hour urine were measured. Blood urea and creatinine levels and urine tubular injury markers were measured. Renal histology was semiquantitatively assessed.Results. Urea, creatinine and urine neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were all increased in Genta group indicating AKI model. Systolic blood pressure decreased, but urine volume and glutathione increased in Genta + Vit D group compared to Control group. Histological scores indicating tubular injury increased in Genta and Genta + Vit D groups.Conclusions. Vitamin D does not seem to be effective on histological findings although it has some beneficial effects via RAS system and a promising effect on antioxidant system.

scholarly journals Urinary N-Acetyl-Beta-D-Glucosaminidase Activity in Rat Experimental Ischemic and Toxic Models of Acute Kidney Injury

2017 ◽  
Vol 74 (1) ◽  
pp. 105
Author(s):  
Razvan Andrei CODEA ◽  
Mircea MIRCEAN ◽  
Sidonia Alina BOGDAN ◽  
Andras Laszlo NAGY ◽  
Alexandra BIRIS ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Experimental Model ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Control Group ◽  
Tubular Injury ◽  
Group 2 ◽  
Group 1

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

scholarly journals Nephroprotective Effects of L-Arginine against Chemotherapy Induced Acute Kidney Injury in Wistar Rats

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 ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Wistar Rats ◽  
Kidney Injury ◽  
Control Group ◽  
P Value ◽  
Renal Histology ◽  
Renal Markers ◽  
Group B ◽  
Experimental Group

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

scholarly journals Impact of Ciprofloxacin With Autophagy on Acute Kidney Injury

2021 ◽  
Author(s):  
Woo Yeong Park ◽  
Sun-Ha Lim ◽  
Yaerim Kim ◽  
Jin Hyuk Paek ◽  
Kyubok Jin ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Beclin 1 ◽  
Control Group ◽  
Renal Tubules ◽  
Tubular Injury ◽  
Renal Tubular Cells ◽  
Renal Tubular

Abstract Renal tubular injury caused by oxidative stress and inflammation results in acute kidney injury. Recent research reported that antibiotics may restore deteriorated renal tubules, but the underlying mechanism remains unclear. Therefore, we investigated the efficacy and mechanism of action of antibiotics against renal tubular injury. We screened ciprofloxacin, ceftizoxime, minocycline, and netilmicin and selected ciprofloxacin to examine further because of its low toxicity towards renal tubular cells. We evaluated the effect of ciprofloxacin on cell survival by analyzing apoptosis and autophagy. TUNEL assay results showed that the ciprofloxacin group had less apoptotic cells than the control group. The ratio of cleaved caspase 3 to caspase 3, the final effector in the apoptosis process, was decreased, but the ratio of Bax to Bcl-2 located upstream of caspase 3 was not decreased in the ciprofloxacin group. Therefore, apoptosis inhibition does not occur via Bax/Bcl-2. Conversely, the levels of phosphorylated Bcl-2, and Beclin-1, an autophagy marker, were increased, and that of caspase-3 was decreased in the ciprofloxacin group. This indicates that ciprofloxacin enhanced autophagy, increasing the amount of free Beclin-1 via phosphorylated Bcl-2, and inhibited caspase activity. Therefore, ciprofloxacin might increase renal cell viability through the autophagy activation in acute kidney injury.

scholarly journals Melatonin mitigates cisplatin-induced acute kidney injury through regulation of the heat shock proteins expressions

2021 ◽  
Author(s):  
Ali Tuğrul Akin ◽  
Murat Unsal ◽  
Tayfun Ceylan ◽  
Emin Kaymak ◽  
Emel Ozturk ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Uric Acid ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Blood Serum ◽  
Renal Cortex ◽  
Kidney Injury ◽  
Control Group ◽  
Albino Rats ◽  
Shock Proteins

Abstract Purpose. To determine the protective effects of melatonin (MEL) in acute kidney injury (AKI) induced by Cisplatin (CP), widely used as a chemotherapeutic in the treatment of many cancer types, via assessment of heat-shock proteins (HSPs) levels in rats. Methods. Total 40 Wistar albino rats were divided into four groups: Control (n = 10), MEL (n = 10, 10 mg/kg/i.p melatonin for 8 days), CP (n = 10, 7 mg/kg/i.p cisplatin at the 5th day), and CP + MEL (n = 10, 10 mg/kg/i.p melatonin for 8 days and 7 mg/kg/i.p cisplatin at the 5th day). After administrations, animals were sacrificed, and kidney tissues were extracted. Histopathological changes were evaluated and glomerular and tubular immunoreactivities of HSP47, HSP60, HSP7, and HSP90 in renal cortex were detected by immunohistochemistry. Moreover, blood serum BUN, creatinine and uric acid levels were measured to assess of kidney function. Results. CP group showed histopathological deterioration compared to Control group and MEL treatment attenuated this damage. When compared with Control and MEL groups, an increase in HSPs immunoreactivities in renal cortex and blood serum BUN, creatinine and uric acid levels were observed in the CP group. Furthermore, an improvement was observed in the CP + MEL in terms of these parameters compared to the CP group. Conclusion. According to our results, MEL could exert a significant protective effect to ameliorate CP-induced AKI via regulation of heat-shock protein expressions.

scholarly journals A Randomized, Double-Blind, Placebo-Controlled, Clinical Trial of High-Dose, Short-Term Vitamin D Administration in the Prevention of Acute Kidney Injury after Cardiac Surgery

2021 ◽  
pp. 1-7
Author(s):  
Pegah Eslami ◽  
Manouchehr Hekmat ◽  
Mahmoud Beheshti ◽  
Ramin Baghaei ◽  
Seyed Mohsen Mirhosseini ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Vitamin D ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Injury ◽  
Control Group ◽  
Controlled Clinical Trial ◽  
High Dose ◽  
Double Blind ◽  
Postoperative Aki

<b><i>Background:</i></b> Acute kidney injury (AKI) after cardiac surgery is a relatively common complication affecting short- and long-term survival. The renoprotective effect of vitamin D (VitD) has been confirmed in several experimental models. This study was conducted to evaluate the effect of high-dose VitD administration in patients with VitD insufficiency on the incidence of postoperative AKI, the urinary level of tubular biomarkers, and serum anti-inflammatory biomarker after coronary artery bypass graft. <b><i>Design and Method:</i></b> In this randomized double-blind controlled clinical trial, the patients were randomly allocated to either the VitD group (<i>n</i> = 50), receiving 150,000 IU VitD tablets daily for 3 consecutive days before surgery or the control group (<i>n</i> = 61), receiving placebo tablets. <b><i>Results:</i></b> There was no difference in the incidence of postoperative AKI between the groups. Both of the urinary levels of interleukin-18 and kidney injury molecule-1 were significantly increased after the operation (<i>p</i> &#x3c; 0.001, for both). Also, the serum level of interleukin-10 was increased after 3 days of VitD supplementation (<i>p</i> = 0.001). In comparison with the control group, it remained on a higher level after the operation (<i>p</i> &#x3c; 0.001) and the next day (<i>p</i> = 0.03). The patients with AKI had more postoperative bleeding and received more blood transfusion. <b><i>Conclusion:</i></b> VitD pretreatment was unable to impose any changes in the incidence of AKI and the urinary level of renal biomarkers. However, high-dose administration of VitD may improve the anti-inflammatory state before and after the operation. Further studies are needed to assess the renoprotective effect of VitD on coronary surgery patients.

scholarly journals The effects of steroidal and non-steroidal anti-inflammatory drugs on tracheal wound healing in an experimental rat model

2020 ◽  
Vol 30 (4) ◽  
pp. 646-651
Author(s):  
Elif Duman ◽  
Kenan Can Ceylan ◽  
Deniz Akpınar ◽  
Nur Yücel ◽  
Şaban Ünsal ◽  
...  
Keyword(s):  
Wound Healing ◽  
Rat Model ◽  
Control Group ◽  
Albino Rats ◽  
Nsaid Group ◽  
Steroid Group ◽  
Histological Characteristics ◽  
Experimental Rat Model ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Abstract OBJECTIVES The effect of non-steroidal anti-inflammatory drugs (NSAID), mostly used for postoperative analgesic purposes for wound healing, is still a matter of debate. Our goal was to evaluate the effects of the most widely used NSAID and corticosteroids after surgical operations on tracheal wound healing in an experimental rat model. METHODS Thirty-nine male Wistar albino rats were included in this study. Tracheotomy was performed in 32 rats; then they were divided into 3 groups. After the first day, the animals in group 1 were treated with an NSAID (diclofenac 10 mg/kg/day) (NSAID, n = 12) for 7 days; the animals in group 2 were treated with a corticosteroid (dexamethasone, 2 × 0.1 mg/kg/day) (steroid, n = 10) for 7 days; the animals in group 3 (control, n = 10) were not given any medications. For a fourth group (histological control, n = 7), in order to evaluate normal morphological and histological characteristics, neither surgery nor medication was used. Five rats were eliminated from the study (2 rats in the NSAID group died and 3 rats in the steroid group developed local wound infections). The drop-out rate was 12.8%. Histological characteristics, inflammation, fibrosis, necrosis, neochondrogenesis, neovascularization and epithelization were evaluated in 34 rats. Non-parametric tests were used for statistical analysis. RESULTS Inflammation, vascularization and number of fibroblasts and chondrocytes were significantly higher in the control group than in the histological control group. There was some reduction in all parameters except vascularization in the NSAID group (P &gt; 0.05). When the steroid group was compared to the NSAID group, inflammation (P &lt; 0.05), vascularization and number of chondrocytes (P &gt; 0.05) were more suppressed in the steroid group. The number of fibroblasts increased in the steroid group (P &gt; 0.05). CONCLUSIONS Steroids and NSAID may have negative effects on tracheal wound healing, probably by suppressing inflammation and fibroblast proliferation. NSAID was mostly used postoperatively for analgesic purposes and should be avoided.

scholarly journals Tongfu Huoxue Decoction Reduces Autophagy and Apoptosis to Protect Against Acute Renal Injury in a Rat Model of Sepsis

2020 ◽  
Author(s):  
Yan Wang ◽  
Zixuan Wang ◽  
Qianlan Yang ◽  
Yuxin Fan ◽  
Lu Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Rat Model ◽  
Renal Injury ◽  
Dose Group ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Control Group ◽  
Acute Renal Injury ◽  
Related Proteins ◽  
Dose Dependent

Abstract Background: To investigate the mechanism by which Tongfu Huoxue decoction protects against acute kidney injury in sepsis in rats, and provide a new therapeutic strategy for clinical intervention.Methods: Thirty-two Sprague–Dawley rats were randomly divided into a control group (saline), model group (lipopolysaccharide LPS group), LPS group+Tongfu Huoxue Decoction high-dose group (H group), and LPS group +Tongfu Huoxue Decoction low-dose group (L group). A rat model of acute kidney injury in sepsis was established by administration of LPS, and Tongfu Huoxue decoction was administered by gavage. The pathological and morphological changes of the kidneys were evaluated according to the levels of urea nitrogen (BUN) and blood creatinine (SCr). The expression of the inflammation-related factors IL-1b, IL-6 and TNF-a was determined by quantitative real-time PCR. Changes in the phosphorylation levels of the autophagy and apoptosis-related proteins LC3, beclin-1, caspase-3 and Akt were detected by Western blot analysis. Results: Compared with the model LPS group, kidney tissue damage was reduced in rats treated with Tongfu Huoxue decoction. The expression levels of inflammation-related and autophagy-related proteins in the kidney tissue of rats treated with Tongfu Huoxue decoction were significantly lower than those in the LPS group, which was showed a dose-dependent decrease in expression. After stimulation of HK-2 cells with LPS, the expression levels of the autophagy and apoptosis in the groups treated with Tongfu Huoxue decoction decreased in a dose-dependent manner. Furthermore, the rate of HK-2 cell apoptosis was higher in the LPS group than that in the control group, with lower rates in the H and L groups than that in the LPS group and were dose-dependent.Conclusion: Tongfu Huoxue decoction protects against acute renal injury in sepsis by reducing autophagy and apoptosis.

Pazopanib-Induced Hepatotoxicity in an Experimental Rat Model

Chemotherapy ◽  
2018 ◽  
Vol 63 (1) ◽  
pp. 39-45
Author(s):  
Bulent Cetin ◽  
Guldal Esendagli Yılmaz ◽  
Berkan Armagan ◽  
Baris Afsar ◽  
Umut Demirci ◽  
...  
Keyword(s):  
Kupffer Cells ◽  
Rat Model ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Control Group ◽  
Albino Rats ◽  
Tissue Samples ◽  
Experimental Rat Model ◽  
Group 3 ◽  
Group 2

Pazopanib is an effective treatment for advanced renal cell carcinoma and soft tissue sarcoma. Besides classical adverse events of this drug class, hepatotoxicity has been described as a frequent side effect. The aim of the present study was to evaluate the effect of pazopanib on the liver in an experimental rat model. Sixteen Wistar albino rats were divided into 3 groups: experimental toxicity was induced with pazopanib (10 mg/kg) administered for 28 days (group 2) or 56 days (group 3) orally by gavage. Group 1 (control group) received only distilled water. Rats in groups 2 and 3 were sacrificed after the collection of blood and tissue samples on the 28th and 56th days, respectively. We found significant differences in bilirubin, alkaline phosphatase, lactate dehydrogenase, glucose, triglyceride, very-low-density lipoprotein, and iron values (p < 0.050 for all) but none in any other parameter (p > 0.050). All rats in the control group had normal histological features; however, none of the rats in groups 2 and 3 showed normal histology. In group 2, we observed mild sinusoidal dilatation, congestion, enlarged Kupffer cells, accumulation of yellow-brown-black pigment in the Kupffer cells and the accumulation of hemosiderin with Prussian blue reaction in the hepatocytes. In group 3, the findings mentioned above were more prominent, and besides these findings focal acinar transformation and macrovesicular steatosis were also observed. In group 3, mild inflammation within the portal areas was observed consisting of lymphocytes, neutrophils, and eosinophils. This study is the first that reports the biochemical and histopathological evaluation of pazopanib-related hepatic toxicity.

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