Abstract 388: Postconditioning Beyond The Heart: Postconditioning The Ischemic Kidney Attenuates Renal Reperfusion Injury

Objective : Postconditioning (Poc), defined as brief cycles of arterial occlusion and reflow applied at the onset of reperfusion (R), has proven to reduce multiple consequences of myocardial ischemia-reperfusion injury (I/R). The protective effects of Poc in the kidney I/R are not known. Therefore, we tested the hypothesis that Poc attenuates renal I/R injury via adenosine receptor (AR) activation and protein kinase C (PKC) signaling. Methods : The in vivo single kidney rat model was used. Rats underwent right nephrectomy and were randomized to 5 groups. A sham group (n=8) underwent the surgical and perfusion protocol without other interventions. In all remaining groups, the left renal artery is occluded for 45min and the left kidney was reperfused for 24 hours. Control group (n=8) received no intervention at R; Poc (n=8) underwent 4 cycles of 45 seconds R and 45 seconds of reocclusion at the onset of R. PC + ARi (n=6): the AR inhibitor 8-SPT (10mg/kg) was administered i.v. 5 minutes before Poc; Poc + PKCi: the PKC inhibitor, chelerytherine (5mg/kg), was administered i.v. 5 min before R. After 24 hours, renal function was assessed by plasma blood urea nitrogen (BUN) and creatinine (Cr), and the kidneys were harvested; apoptotic cells were quantified by TUNEL stain and morphological injury by H&E staining. Results: Compared to sham, BUN and Cr were greater in control I/R group, which was significantly reduced in Poc (table ). Inhibition of AR or PKC stimulation reversed the reductions in BUN and Cr achieved by Poc. In addition, renal I/R increased the percentage of TUNEL positive cells in ten high powered fields vs Sham, which was reduced by Poc. Blockade of AR and PKC reversed the apoptosis reduction achieved by Poc. Conclusion: Postconditioning attenuates renal dysfunction and apoptosis induced by R injury and involves AR and PKC signaling. Poc suggests that R injury is triggered in early moments of reflow.

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Protective effects of hydrogen on oxidative stress and liver function during CO2 pneumoperitoneum in dogs

Medycyna Weterynaryjna ◽

10.21521/mw.6459 ◽

2020 ◽

Vol 76 (10) ◽

pp. 6459-2020

Author(s):

JIANTAO ZHANG ◽

XIAOYAN ZHENG ◽

LIHONG JIANG ◽

TAO ZE ◽

TAO LIU

Keyword(s):

Oxidative Stress ◽

Liver Function ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Hydrogen Gas ◽

Intraabdominal Pressure ◽

Control Group ◽

Protective Effects ◽

Co2 Pneumoperitoneum

The purpose of this study was to investigate the protective effects of hydrogen reducing ischemia-reperfusion injury during CO2 pneumoperitoneum on oxidative stress and liver function. Eighteen healthy Beagle dogs were divided into three groups. Dogs in the control group were subjected only to anesthesia for 90 min. The pneumoperitoneum group was subjected to the pressure of CO2 pneumoperitoneum with 12 mmHg intraabdominal pressure for 90 min. The hydrogen group was subjected to the pressure of CO2 pneumoperitoneum with 12 mmHg intra-abdominal pressure for 90 min after a subcutaneous injection of hydrogen gas (0.2 mL/kg) for 10 min. Blood samples were collected before the induction of pneumoperitoneum, as well as 2 h and 6 h after deflation, to evaluate oxidative stress and liver function in serum. Liver tissue samples were taken 6 h after deflation for histopathological examination. In comparison with group P, a milder histopathological change was found in group H2, and the levels of hepatic function and anti-oxidation in group H2 were higher. Hydrogen gas reduced liver ischemia-reperfusion injury due to CO2 pneumoperitoneum by reducing oxidative stress and improving liver function. Hydrogen gas therapy can be considered as a way to reduce liver ischemiareperfusion injury in laparoscopic surgery.

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Effect of sildenafil in renal ischemia/reperfusion injury in rats

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502010000600006 ◽

2010 ◽

Vol 25 (6) ◽

pp. 490-495 ◽

Cited By ~ 24

Author(s):

Paulo José de Medeiros ◽

Arthur Villarim Neto ◽

Francisco Pignataro Lima ◽

Ítalo Medeiros Azevedo ◽

Layra Ribeiro de Sousa Leão ◽

...

Keyword(s):

Ischemia Reperfusion Injury ◽

Histopathological Examination ◽

Ischemia Reperfusion ◽

Left Kidney ◽

Renal Ischemia ◽

Renal Scintigraphy ◽

Control Group ◽

Left Renal Artery ◽

Differential Function ◽

The Right

PURPOSE: To evaluate the effect of sildenafil, administered prior to renal ischemia/reperfusion (I/R), by scintigraphy and histopathological evaluation in rats. METHODS: Twenty-four rats were divided randomly into two groups. They received 0.1 ml of 99mTechnetium-etilenodicisteine intravenous, and a baseline (initial) renal scintigraphy was performed. The rats underwent 60 minutes of ischemia by left renal artery clamping. The right kidney was not manipulated. The sildenafil group (n=12) received orally 1 mg/kg of sildenafil suspension 60 minutes before ischemia. Treatment with saline 0.9% in the control group (n=12). Half of the rats was assessed after 24 hours and half after seven days I/R, with new renal scintigraphy to study differential function. After euthanasia, kidneys were removed and subjected to histopathological examination. For statistical evaluation, Student t and Mann-Whitney tests were used. RESULTS: In the control group rats, the left kidneys had significant functional deficit, seven days after I/R, whose scintigraphic pattern was consistent with acute tubular necrosis, compared with the initial scintigraphy (p<0.05). Sildenafil treatment resulted in better differential function of the left kidneys 24h after reperfusion, compared with controls. Histopathologically, the left kidney of control rats (24 hours after I/R) showed a higher degree of cellular necrosis when compared with the sildenafil treated rats (p<0.05). CONCLUSION: Sildenafil had a protective effect in rat kidneys subjected to normothermic I/R, demonstrated by scintigraphy and histomorphometry.

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Renal ischemia and reperfusion injury: influence of chorpromazine on renal function and lipid peroxidation

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502008000700008 ◽

2008 ◽

Vol 23 (suppl 1) ◽

pp. 42-46 ◽

Cited By ~ 5

Author(s):

Silvio Tucci Junior ◽

Roberto Marins de Carvalho ◽

Fábia Martins Celini ◽

Adauto José Cologna ◽

Haylton Jorge Suaid ◽

...

Keyword(s):

Lipid Peroxidation ◽

Renal Function ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Left Kidney ◽

Renal Ischemia ◽

Control Group ◽

Ischemia And Reperfusion Injury ◽

Mda Content

PURPOSE: To evaluate the influence of chlorpromazine (CPZ) on renal function and lipid peroxidation in a rat model of kidney ischemia/reperfusion injury. METHODS: Forty eight Wistar rats underwent a laparotomy for hilar clamping of left kidney with a bulldog clamp for 60 minutes followed by organ reperfusion and contralateral nephrectomy. Of these, 26 received 3mg/kg of CPZ intravenously 15 minutes before renal ischemia (G-E) while the remaining 22 were used as ischemic control group (G-C). Eleven rats of G-E and 8 of G-C were followed for blood urea nitrogen and creatinine determinations before renal ischemia and at 1st, 4th and 7th postoperative days. Samplings of left renal tissue were obtained at 5 minutes (5 rats from each group) and 24 hours (9 G-C and 10 of G-E) of reperfusion for malondialdehy (MDA) content determination. Controls of renal MDA content were determined in kidneys harvested from 6 additional normal rats. RESULTS: Acute renal failure occurred in all animals but levels of BUN and creatinine were significantly lower in G-E (p<0.001). MDA content rose strikingly at 5 minutes of reperfusion in both groups (p>0.05) and returned near to normal levels 24 hours later. CONCLUSION: CPZ conferred partial protection of renal function to kidneys submitted to ischemia/reperfusion injury that seems to be not dependent on inhibition of lipid peroxidation.

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Protective Effects of Atractylodes macrocephala Polysaccharide on Liver Ischemia–Reperfusion Injury and Its Possible Mechanism in Rats

The American Journal of Chinese Medicine ◽

10.1142/s0192415x11008981 ◽

2011 ◽

Vol 39 (03) ◽

pp. 489-502 ◽

Cited By ~ 12

Author(s):

Cheng Jin ◽

Pei-Jian Zhang ◽

Chuan-Qing Bao ◽

Yuan-Long Gu ◽

Bing-Hua Xu ◽

...

Keyword(s):

Reperfusion Injury ◽

Normal Control ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Treated Group ◽

Normal Control Group ◽

Control Group ◽

Therapeutic Effects ◽

Protective Effects ◽

Atractylodes Macrocephala

Atractylodes macrocephala polysaccharide (AMP), a traditional Chinese medicine, is thought to have protective effects against liver injury. Therefore, this study was designed to explore the effects of AMP on hepatic ischemia–reperfusion injury (IRI) and elucidate the possible mechanisms. Ninety-six Sprague-Dawley rats were randomly divided into four groups with 24 rats per group: a normal control group, an IRI group, an AMP-treated group (0.4 g/kg/d) and a bifendate-treated group (100 mg/kg). Rats were treated with AMP or bifendate once daily for seven days by gastric gavage. The normal control group and the IRI model group received an equivalent volume of physiological saline. At 1, 6 and 24 h after surgery, the rats were killed and liver tissue samples were obtained to determine interleukin-1 (IL-1) expression by Western blotting and nuclear factor-κB (NF-κB) expression by immunohistochemistry. Liver morphology was assessed by microscopy and transmission electron microscopy. Blood samples were obtained to measure liver function (alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin). AMP significantly reduced the elevated expression of markers of liver dysfunction and the hepatic morphologic changes induced by hepatic IRI in rats. AMP also markedly inhibited IRI-induced lipid peroxidation and altered the activities of the antioxidant enzyme superoxide dismutase and malondialdehyde levels. Moreover, pretreatment with AMP suppressed the expression of interleukin-1β and NF-kB in IRI-treated rats. These results suggest that AMP exerts protective and therapeutic effects against hepatic IRI in rats, which might be associated with its antioxidant properties and inhibition of NF-κB activation. More studies are needed to better understand the mechanisms underlying the protective effects of AMP on hepatic IRI.

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Melatonin and Glycine Reduce Uterus Ischemia/Reperfusion Injury in a Rat Model of Warm Ischemia

International Journal of Molecular Sciences ◽

10.3390/ijms22168373 ◽

2021 ◽

Vol 22 (16) ◽

pp. 8373

Author(s):

Viktorija Zitkute ◽

Mindaugas Kvietkauskas ◽

Vygante Maskoliunaite ◽

Bettina Leber ◽

Diana Ramasauskaite ◽

...

Keyword(s):

Reperfusion Injury ◽

Rat Model ◽

Ischemia Reperfusion Injury ◽

Cell Damage ◽

Ischemia Reperfusion ◽

Combined Treatment ◽

Warm Ischemia ◽

Control Group ◽

Protective Effects ◽

Sprague Dawley

Ischemia/reperfusion injury (IRI) remains a significant problem to be solved in uterus transplantation (UTx). Melatonin and glycine have been shown to possess direct cytoprotective activities, mainly due to their antioxidative and anti-inflammatory properties. The aim of this study was to investigate the protective effects of melatonin and glycine and their combination on IRI in a rat model of warm ischemia. In this study, Sprague-Dawley rats were assigned to eight groups, including sham and IRI (n = 80). Melatonin and glycine alone or their combination were administered prior to 1 h of uterus ischemia followed by 1 h of reperfusion. Melatonin (50 mg/kg) was administered via gavage 2 h before IRI and glycine in an enriched diet for 5 days prior to intervention. Uterus IRI was estimated by histology, including immunohistochemistry, and biochemical tissue analyses. Histology revealed that uterus IRI was significantly attenuated by pretreatment with melatonin (p = 0.019) and glycine (p = 0.044) alone as well as their combination (p = 0.003). Uterus IRI led to increased myeloperoxidase expression, which was significantly reduced by melatonin (p = 0.004), glycine (p < 0.001) or their combination (p < 0.001). The decline in superoxide dismutase activity was significantly reduced in the melatonin (p = 0.027), glycine (p = 0.038) and combined treatment groups (p = 0.015) when compared to the IRI control group. In conclusion, melatonin, glycine and their combination significantly reduced oxidative stress-induced cell damage after IRI in a small animal warm ischemia model, and, therefore, clinical studies are required to evaluate the protective effects of these well-characterized substances in uterus IRI.

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Prevention of renal ischemia/reperfusion injury in rats using acetylcysteine after anesthesia with isoflurane

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502012000400010 ◽

2012 ◽

Vol 27 (4) ◽

pp. 340-345 ◽

Cited By ~ 8

Author(s):

André Marques Mansano ◽

Pedro Thadeu Galvão Vianna ◽

Viciany Erique Fabris ◽

Leopoldo Muniz da Silva ◽

Leandro Gobbo Braz ◽

...

Keyword(s):

Serum Creatinine ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Isotonic Saline ◽

Renal Ischemia ◽

Control Group ◽

Left Renal Artery ◽

Anesthesia Induction ◽

Tubular Necrosis

PURPOSE: To evaluate the effect of N-acetylcysteine, as a renoprotective agent, when administered early after anesthesia induction, against ischemia/reperfusion injury in rats anesthetized with isoflurane. METHODS: Eighteen male Wistar rats weighing > 300g were anesthetized with isoflurane. The internal jugular vein and the left carotid artery were dissected and cannulated. The animals were randomly divided into GAcetyl, receiving intravenous N-acetylcysteine, 300mg/kg, and GIsot, isotonic saline. After 30 minutes, right nephrectomy was performed and the left renal artery was clamped during 45 minutes. The animals were sacrificed after 48 hours and blood samples were taken after anesthetic induction and upon sacrificing of the animals to evaluate blood creatinine. The kidneys were sent for histological analysis. RESULTS: The variation in serum creatinine was 2.33mg/dL ± 2.21 in GAcetyl and 4.38mg/dL ± 2.13 in GIsot (p=0.074). Two animals presented intense tubular necrosis in GAcetyl, compared to 5 in GIsot. Only GAcetyl presented animals free of tubular necrosis (two) and tubular degeneration (one). CONCLUSION: After renal ischemia/reperfusion, the rats which were given N-acetylcysteine presented less variation in serum creatinine and milder kidney injuries than the control group.

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Selenium effects on antioxidant and inflammatory indices in renal ischemia-reperfusion injury in rats

Journal of Renal Injury Prevention ◽

10.15171/jrip.2019.14 ◽

2018 ◽

Vol 8 (2) ◽

pp. 71-77 ◽

Cited By ~ 2

Author(s):

Hassan Ahmadvand ◽

Esmaeel Babaeenezhad ◽

Hashem Nayeri ◽

Zahra Zarei Nezhad

Keyword(s):

Oxidative Stress ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Left Kidney ◽

Serum Levels ◽

Renal Ischemia ◽

Paraoxonase 1 ◽

Control Group ◽

Protective Effects ◽

Oxidative Stress Biomarkers

Introduction: Selenium (Se) is an antioxidant and reactive oxygen species (ROS) scavenger. Objectives: This study was conducted to evaluate the effects of Se on renal functional parameters, oxidative stress biomarkers, myeloperoxidase (MPO) activity, and the nitric oxide (NO) level in renal ischemia-reperfusion (IR) injury in rats. Materials and Methods: Twenty-four male Wistar rats (180–200 g) were selected and subsequently divided into three groups (n=8); group 1 as the control group, group 2 as the untreated group (IR without treatment) and group 3 as the IR group (treated with Se (1 mg/kg/d, intraperitoneally). The period of Se administration was 2 weeks before the inducing renal IR. To cause renal IR, renal pedicles were occluded by safe clamps for 45 minutes. Then, the clamps were removed and 24 hours was considered as reperfusion. After the study, blood sampling from the hearts and the removal of the left kidney was conducted immediately for biochemical measurements. Results: Renal IR significantly increased serum levels of urea, creatinine (Cr), serum and renal malondialdehyde (MDA) levels, serum NO level, and MPO activity. It significantly decreased serum and renal glutathione (GSH) levels, serum paraoxonase 1 activity, serum and renal activities of catalase (CAT), and glutathione peroxidase (GPx). Se could reverse these findings, but the increase of paraoxonase 1 activity and the decrease of MPO activity in IR animals were not significant. Conclusion: It seems that Se has protective effects on inflammatory indices. It can ameliorate renal IR complications which are associated with oxidative stress and inflammation.

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Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

Combinatorial Chemistry & High Throughput Screening ◽

10.2174/1386207323666200219121600 ◽

2020 ◽

Vol 23 (3) ◽

pp. 214-224 ◽

Cited By ~ 1

Author(s):

Esra Cakir ◽

Ufuk Cakir ◽

Cuneyt Tayman ◽

Tugba Taskin Turkmenoglu ◽

Ataman Gonel ◽

...

Keyword(s):

Cerebral Ischemia ◽

Reperfusion Injury ◽

Brain Damage ◽

Neurological Deficit ◽

Cell Apoptosis ◽

Ischemia Reperfusion Injury ◽

Degradation Products ◽

Ischemia Reperfusion ◽

Control Group ◽

Cortex Cell

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.

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