scholarly journals Calcitriol and Erythropoietin Protect Against Cardiac Injury Induced by Renal Ischemia-Reperfusion

2020 ◽  
Vol 10 (6) ◽  
pp. 6718-6727 ◽  
Keyword(s):  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Renal Ischemia ◽  
Albino Rats ◽  
Cardiac Damage ◽  
Beneficial Effects ◽  
Tubular Necrosis ◽  
Wistar Albino Rats

Cardiac abnormalities and dysfunction are the most important complications after renal ischemia-reperfusion (IR). Thus, investigation and development of effective treatment to decrease cardiac damage induced by renal ischemia are necessary. This study examined the effects of treatment with calcitriol and erythropoietin (EPO) on cardiac injury induced by renal ischemia. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion, followed by 24 h reperfusion. Calcitriol and EPO were administered before ischemia. After 24 h reperfusion, blood samples were collected for the determination of biochemical parameters, and kidney and cardiac samples were taken for histological studies. Renal IR increased BUN-Cr levels, lipid profiles, and myocardial injury markers (CK-MB and LDH). Histopathological findings of the IR group confirmed that there were glomerular atrophy and acute tubular necrosis in the renal tissues and lymphocyte infiltration and intercellular edema in the cardiac samples. Treatment with calcitriol and EPO boosted cardiac and renal functions and improved the morphological changes. It seems that calcitriol or EPO administration could protect against the kidney and cardiac damage induced by IR. Also, the combination of calcitriol and EPO may exert more beneficial effects than either agent used alone.

scholarly journals Protective effect of vitamin D3 and erythropoietin on renal ischemia/reperfusion-induced liver and kidney damage in rats

2020 ◽  
Vol 9 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Mohammad-ghasem Golmohammadi ◽  
Reza Ajam ◽  
Ali Shahbazi ◽  
Mir Mehdi Chinifroush-Asl ◽  
Shokofeh Banaei
Keyword(s):  
Vitamin D ◽  
Liver Damage ◽  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Dihydroxyvitamin D3 ◽  
Beneficial Effects ◽  
Tubular Necrosis ◽  
Liver And Kidney ◽  
Kidney Functions

Introduction: Renal ischemia reperfusion (IR) contributes to the development of acute renal failure (ARF). Free radicals are considered to be principal components involved in the pathophysiological alterations observed during IR. In this study, we evaluated the effects of vitamin D and erythropoietin (EPO) in IR–induced renal and liver damage. Methods: Wistar rats were divided into five groups of 6 each. 1) The control, 2) IR, 3) VD3 (1,25-dihydroxyvitamin D3) + IR, 4) EPO+ IR, and 5) VD3+EPO+ IR groups. The rats were unilaterally nephrectomized and subjected to 45 minutes of renal pedicle occlusion followed by 24 h reperfusion. Vitamin D (10 mg/kg, IP) and EPO (1000 U/kg, IP) were administered prior to ischemia. After 24 hours reperfusion, the blood samples were collected for the determination of biochemical parameters and kidney and liver samples were taken for histological studies. Results: Renal ischemia significantly decreased kidney and liver functions. IR significantly increased blood urea nitrogen-creatinine (BUN-Cr), glucose, total protein and liver enzyme levels and significantly decreased hemoglobin (Hb) and hematocrit (Hct) values. Histopathological findings of the IR group confirmed that there were glomerular atrophy and acute tubular necrosis in the renal tissues and lymphocyte infiltration in the liver samples. Treatment with vitamin D and EPO boosted liver and kidney functions and improved the morphological changes. Conclusion: It seems that vitamin D or EPO administration could protect the kidney and liver damage induced by IR. Also, the combination of vitamin D and EPO may exert more beneficial effects than either agent used alone.

The proteasome inhibitor Bortezomib aggravates renal ischemia-reperfusion injury

2009 ◽  
Vol 297 (2) ◽  
pp. F451-F460 ◽  
Author(s):  
Julia M. Huber ◽  
Andrea Tagwerker ◽  
Dorothea Heininger ◽  
Gert Mayer ◽  
Alexander R. Rosenkranz ◽  
...  
Keyword(s):  
T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Reversible Inhibitor ◽  
Tubular Necrosis ◽  
Proinflammatory Mediators ◽  
Renal Ischemia Reperfusion Injury ◽  
A Cell

Bortezomib is a well-established treatment option for patients with multiple myeloma (MM). It is a selective and reversible inhibitor of the proteasome that is responsible for the degradation of many regulatory proteins that are involved in apoptosis, cell-cycle regulation, or transcription. Because patients with MM are prone to develop acute renal failure, we evaluated the influence of Bortezomib on renal ischemia-reperfusion injury (IRI). Mice were subjected to renal IRI by having the renal pedicles clamped for 30 min followed by reperfusion for 3, 24, and 48 h. Mice were either pretreated with 0.5 mg/kg body wt Bortezomib or vehicle intravenously 12 h before induction of IRI. Serum creatinine and tubular necrosis were significantly increased in Bortezomib compared with vehicle-treated mice. The inflammatory response was found to be significantly decreased in Bortezomib-treated mice as reflected by a decreased infiltration of CD4+ T cells and a significantly decreased Th1 cytokine expression in the kidneys. In contrast, apoptosis was significantly increased in kidneys of Bortezomib-treated mice compared with vehicle-treated controls. Increased numbers of TUNEL-positive cells/mm2 and increased mRNA expression of proapoptotic factors were detected in kidneys of Bortezomib-treated mice. Of note, p21, a cell senescence marker, was also significantly increased in kidneys of Bortezomib-treated mice. In summary, we provide evidence that Bortezomib worsens the outcome of renal IRI by leading to increased apoptosis of tubular cells despite decreased infiltrating T cells and proinflammatory mediators.

scholarly journals ROLE OF OCIMUM CANUM IN PREVENTION OF REPERFUSION-INDUCED RENAL ISCHEMIA IN WISTAR ALBINO RATS

2012 ◽  
Vol 3 (7) ◽  
Author(s):  
Saiprasanna Behera ◽  
S M Babu ◽  
Y Roja Ramani ◽  
Prasanta Kumar Choudhury ◽  
Sudeep Kumar Patra
Keyword(s):  
Renal Ischemia ◽  
Albino Rats ◽  
Wistar Albino Rats

The Beneficial Effects of Tadalafil on Renal Ischemia-Reperfusion Injury in Rats

2011 ◽  
Vol 86 (2) ◽  
pp. 197-203 ◽  
Author(s):  
Mehmet Guzeloglu ◽  
Fatih Yalcinkaya ◽  
Soner Atmaca ◽  
Alper Bagriyanik ◽  
Suleyman Oktar ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Beneficial Effects ◽  
Renal Ischemia Reperfusion Injury

Can N-Acetylcysteine Preserve Peritoneal Function and Morphology in Encapsulating Peritoneal Sclerosis?

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 202-205 ◽  
Author(s):  
Devrim Bozkurt ◽  
Ender Hur ◽  
Burcu Ulkuden ◽  
Murat Sezak ◽  
Hasim Nar ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Cell Count ◽  
Degradation Products ◽  
Isotonic Saline ◽  
Control Group ◽  
Albino Rats ◽  
Peritoneal Fibrosis ◽  
Beneficial Effects ◽  
Group 2 ◽  
Wistar Albino Rats

Long-term use of the peritoneum as a dialysis membrane results in progressive irreversible dysfunction, described as peritoneal fibrosis. Oxidative stress during peritoneal dialysis has been established in many studies. Generation of reactive oxygen species (ROS) by conventional peritoneal dialysis solutions, regardless of whether produced by high glucose, angiotensin II, or glucose degradation products may be responsible for progressive membrane dysfunction. The well-known antioxidant molecule N-acetylcysteine (NAC) is capable of direct scavenging of ROS. The aim of the present study was to investigate the effect of NAC therapy on both progression and regression of encapsulating peritoneal sclerosis (EPS). We divided 49 nonuremic Wistar albino rats into four groups: Control group—2 mL isotonic saline intraperitoneally (IP) daily for 3 weeks; CG group—2 mL/200 g 0.1% chlorhexidine gluconate (CG) and 15% ethanol dissolved in saline injected IP daily for a total of 3 weeks; Resting group—CG (weeks 1 – 3), plus peritoneal resting (weeks 4 – 6); NAC-R group—CG (weeks 1 – 3), plus 2 g/L NAC (weeks 4 – 6). At the end of the experiment, all rats underwent a 1-hour peritoneal equilibration test with 25 mL 3.86% PD solution. Dialysate-to-plasma ratio (D/P) urea, dialysate white blood cell count (per cubic milliliter), ultrafiltration (UF) volume, and morphology changes of parietal peritoneum were examined. The CG group progressed to encapsulating peritoneal sclerosis, characterized by loss of UF, increased peritoneal thickness, inflammation, and ultimately, development of fibrosis. Resting produced advantages only in dialysate cell count; with regard to vascularity and dialysate cell count, NAC was more effective than was peritoneal rest. Interestingly, we observed no beneficial effects of NAC on fibrosis. That finding may be a result of our experimental severe peritoneal injury model. However, decreased inflammation and vascularity with NAC therapy were promising results in regard to membrane protection.

scholarly journals Protective effects of tempol in an experimental ovarian ischemia–reperfusion injury model in female Wistar albino rats

2017 ◽  
Vol 95 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Neslihan Pınar ◽  
Oya Soylu Karapınar ◽  
Oğuzhan Özcan ◽  
Esin Atik Doğan ◽  
Suphi Bayraktar
Keyword(s):  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Index ◽  
Albino Rats ◽  
Protective Effects ◽  
Group V ◽  
Group Iii ◽  
Group I ◽  
Wistar Albino Rats

The aim of this study was to investigate the antioxidant effects of tempol on ovarian ischemia–reperfusion (I/R) injury in rats. Forty female Wistar albino rats were randomly divided into 5 groups: Group I, sham; Group II, ischemia (I); Group III, I/R; Group IV, I/R + tempol 30 mg/kg i.p; Group V, I/R + tempol 50 mg/kg i.p. Oxidative stress index (OSI) was significantly higher in the ischemia group and the I/R group than in the sham group. Catalase levels were significantly lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. Glutathione peroxidase levels were lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. MDA levels were significantly lower in the I/R + tempol 30 mg/kg i.p. group and the I/R + tempol 50 mg/kg i.p. group than in the I/R group. The levels of the histopathological parameters were significantly decreased in the I/R + tempol 50 mg/kg i.p. group compared with the I/R group. Tempol can be used for reducing ovarian I/R injury.

scholarly journals Effects of Cilostazol and Diltiazem Hydrochloride on Ischemia-Reperfusion Injury in a Rat Hindlimb Model

2017 ◽  
Vol 20 (2) ◽  
pp. 058 ◽  
Author(s):  
Bekir İNAN ◽  
Selma SÖNMEZ ERGÜN ◽  
Asiye NURTEN ◽  
Canan KÜÇÜKGERGİN ◽  
Aslı ZENGİN TÜRKMEN ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Saline Group ◽  
Dimethyl Sulphoxide ◽  
Control Group ◽  
Albino Rats ◽  
Diltiazem Hydrochloride ◽  
Beneficial Effects ◽  
Group I

Objective: Free radicals and neutrophils are potent sources of ischemia-reperfusion injury (I/R) and they can be limited by the use of exogenous application of some therapeutic agents. The objective of this study was to compare the effects of cilostazol and diltiazem hydrochloride in a rat hind limb model of I/R injury. Methods: Skeletal muscles submitted to 2 hours of ischemia by placing an aneurysm clip to femoral artery and reperfused after 1, 2 and 4 hours. Seventy-two Wistar-Albino rats were randomly divided into mainly four groups according to treatment agents:  Group I (control group) was treated with saline; Group II was treated with diltiazem hydrochloride; Group III was treated with cilostazol in 30% dimethyl sulphoxide; and Group IV was treated with 30% dimethyl sulphoxide intraperitoneally. These four main groups also subdivided into three subgroups according to duration of the reperfusion times.  Blood samples were taken and all rats were sacrificed. Results: Cilostazol-treated groups demonstrated a significant decrease in tissue and serum malondialdehyde (MDA) levels, and tissue myeloperoxidase (MPO ) activity compared with other groups. Increase in serum nitric oxide (NOx) level was significantly higher in all subgroups of cilastazol, diltiazem hydrochloride, and dimethyl sulphoxide groups versus the control group.Conclusion: Although these results suggest the beneficial effects of cilostazol and diltiazem hydrochloride on I/R injury, the effect of cilostazol on I/R injury seems to be more efficient than diltiazem hydrochloride.

scholarly journals Tubular Necrosis, Acid-Base and Electrolyte Abnormalities Associated with Gasoline Vapour-induced Nephrotoxicity

2020 ◽  
Vol 2 (3) ◽  
Keyword(s):  
Renal Function ◽  
Biochemical Markers ◽  
Histopathological Examination ◽  
Albino Rats ◽  
Renal Vasculature ◽  
Tubular Necrosis ◽  
Serum Biochemical ◽  
Group 2 ◽  
Wistar Albino Rats ◽  
Electrolyte Abnormalities

Introduction: This study aimed to assess the effect of exposure to gasoline vapor (GV) on the histomorphology and biochemical markers of renal function in rats. Methods: Twenty-four mature Wistar Albino rats weighing 180–200 g were randomly divided into two groups (n = 12 per group). Animals in group 1 (G1) served as unexposed controls, while animals in group 2 (G2) were exposed to GV for 35 days. At the end of the exposure, the animals were sacrificed, and blood samples were collected for biochemical analysis while the kidneys were removed and processed for histopathological evaluation. Results: Serum biochemical markers of renal function in the exposed group differed significantly (p< 0.05) from the unexposed group in urea (45.16 ± 1.00mg/dl versus(vs) 13.20 ± 0.69 mg/dl), creatinine (1.16 ± 0.27mg/dl vs 0.38 ± 0.10mg/dl), uric acid (3.66 ± 0.82mmol/L vs 1.96 ± 0.08mmol/L), potassium (6.90 ± 0.27mmol/L vs 3.57 ± 0.26mmol/L), sodium (182.60 ± 3.21mmol/L vs 141.33 ± 10.46mmol/L), chloride (119.00 ± 1.58mmol/L vs 103.33 ± 2.07mmol/L), pH (6.82 ± 0.22 vs 7.38 ± 0.25), bicarbonate (16.60 ± 5.03mmol/L vs 26.50 ± 3.45mmol/L), and glucose (125.60 ± 16.23mg/ dl vs 83.33 ± 4.46mg/dl). Histopathological examination of kidney sections revealed areas of degenerative and necrotic changes in the glomerulus, tubules, and renal vasculature, particularly in the cortical portion of the kidney. Conclusion: Chronic exposure to gasoline compounds may be associated with significant structural and biochemical derangements in kidney function.

scholarly journals Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats

2018 ◽  
Vol 61 (4) ◽  
pp. 144-149 ◽  
Author(s):  
Aysel Kurt ◽  
Yildiray Kalkan ◽  
Hasan Turut ◽  
Medine Cumhur Cure ◽  
Levent Tumkaya ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Ischemia Reperfusion ◽  
Lung Damage ◽  
Male Rats ◽  
Albino Rats ◽  
Ros Generation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ros Formation ◽  
Wistar Albino Rats

Background: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. Materials and Methods: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. Results: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group’s lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. Conclusions: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.

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