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

2018 ◽  
Vol 8 (2) ◽  
pp. 71-77 ◽  
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.

scholarly journals Glutathione ameliorates liver markers, oxidative stress and inflammatory indices in rats with renal ischemia reperfusion injury

2018 ◽  
Vol 8 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Hassan Ahmadvand ◽  
Esmaeel Babaeenezhad ◽  
Maryam Nasri ◽  
Leila Jafaripour ◽  
Reza Mohammadrezaei Khorramabadi
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Renal Ischemia ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Control Group ◽  
Group I ◽  
Liver Markers

Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR significantly decreased the serum and renal levels of GSH, serum paraoxonase 1 (PON1) activity, and the serum and renal activities of catalase (CAT) and glutathione peroxidase (GPX). GSH administration could significantly improve the serum activities of AST, GGT, MPO, GPX and PON1 and serum levels of NO, renal MDA, GSH levels, and serum and also renal CAT activities. Conclusion: Our study indicated that GSH administration ameliorated RIR injury in rats by improving the activities of liver markers and antioxidant enzymes, the levels of MDA, NO, GSH and MPO activity.

scholarly journals Antioxidative and anti-inflammatory impact of valsartan against renal ischemia-reperfusion injury; role of nitric oxide signaling pathway

2019 ◽  
Vol 5 (2) ◽  
pp. e19-e19
Author(s):  
Leila Mohmoodnia ◽  
Sarina Safari Ahmadvand ◽  
Sahar Koushki ◽  
Behrooz Farzan ◽  
Sajad Papi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Renal Ischemia ◽  
Control Group ◽  
Type I ◽  
Angiotensin Receptor ◽  
Renal Ischemia Reperfusion Injury ◽  
Control Group Group

Introduction: Renal ischemia reperfusion injury is one of the main causes of acute renal failure, which is associated with high mortality. Tissue damage caused by ischemia-reperfusion occurs due to the release of oxygen free radicals. Type I angiotensin receptor antagonists such as valsartan can be useful in the treatment of chronic kidney disease and hypertension. Objectives: We aimed to evaluate the protective effect of valsartan against renal ischemia reperfusion via antioxidant property and nitric oxide (NO) signaling pathway. Materials and Methods: Fifty male Wistar rats (220±10 g) were randomly divided into five groups as follows: Group 1; healthy rats without ischemia-reperfusion (control group). Group 2; rats with ischemia reperfusion (IR) (IR control group). Group 3; rats with IR which received 30 mg/kg valsartan orally. Group 4; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-NAME. Group 5; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-arginine. To induce ischemia-reperfusion, rats were anesthetized with thiopental and underwent surgery. Then, we induced ischemia with blocking blood vessels for 45 minutes by clamping. Biochemical parameters including urea and creatinine were measured using commercial kits. Oxidative stress and inflammatory parameters were measured by ELISA method. Renal tissues were stained with hematoxylin and eosin. Finally, the Kolmogorov-Smirnov test was used to determine the normal distribution of data. Results: The findings of this study indicated that treatment with valsartan and valsartan plus L-arginine leads to significant decrease in the serum levels of creatinine, urea, and albumin/creatinine, malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in contrast to IR control group which has increased level of these parameters. On the other hand, treatment with valsartan and valsartan plus L-arginine lead to increase in the serum levels of glutathione peroxidase (GPX), in contrast to ischemia reperfusion control group. Conclusion: Our data revealed that valsartan as a type I angiotensin receptor antagonist could decrease oxidative stress and inflammation due to renal ischemia reperfusion injury. Hence, valsartan could propose as a therapeutic agent for kidney diseases such as renal ischemia-reperfusion injury regarded to these renoprotective effects.

scholarly journals Lingonberry anthocyanins protect cardiac cells from oxidative-stress-induced apoptosis

2017 ◽  
Vol 95 (8) ◽  
pp. 904-910 ◽  
Author(s):  
Cara K. Isaak ◽  
Jay C. Petkau ◽  
Heather Blewett ◽  
Karmin O ◽  
Yaw L. Siow
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Control Group ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Induced Apoptosis ◽  
Hoechst Staining

Lingonberry grown in northern Manitoba, Canada, contains exceptionally high levels of anthocyanins and other polyphenols. Previous studies from our lab have shown that lingonberry anthocyanins can protect H9c2 cells from ischemia–reperfusion injury and anthocyanin-rich diets have been shown to be associated with decreased cardiovascular disease and mortality. Oxidative stress can impair function and trigger apoptosis in cardiomyocytes. This study investigated the protective effects of physiologically relevant doses of lingonberry extracts and pure anthocyanins against hydrogen-peroxide-induced cell death. Apoptosis and necrosis were detected in H9c2 cells after hydrogen peroxide treatment via flow cytometry using FLICA 660 caspase 3/7 combined with YO-PRO-1 and then confirmed with Hoechst staining and fluorescence microscopy. Each of the 3 major anthocyanins found in lingonberry (cyanidin-3-galactoside, cyanidin-3-glucoside, and cyanidin-3-arabinoside) was protective against hydrogen-peroxide-induced apoptosis in H9c2 cells at 10 ng·mL−1 (20 nmol·L−1) and restored the number of viable cells to match the control group. A combination of the 3 anthocyanins was also protective and a lingonberry extract tested at 3 concentrations produced a dose-dependent protective effect. Lingonberry anthocyanins protected cardiac cells from oxidative-stress-induced apoptosis and may have cardioprotective effects as a dietary modification.

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

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.

scholarly journals Effect of sildenafil in renal ischemia/reperfusion injury in rats

2010 ◽  
Vol 25 (6) ◽  
pp. 490-495 ◽  
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.

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

2008 ◽  
Vol 23 (suppl 1) ◽  
pp. 42-46 ◽  
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.

scholarly journals Oil-In-Water Microemulsion Encapsulation of Antagonist Drugs Prevents Renal Ischemia-Reperfusion Injury in Rats

2021 ◽  
Vol 11 (3) ◽  
pp. 1264
Author(s):  
Parisa Hasanein ◽  
Abbas Rahdar ◽  
Mahmood Barani ◽  
Francesco Baino ◽  
Siamak Yari
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Kidney Damage ◽  
Control Group ◽  
Water Type ◽  
Beneficial Effects ◽  
Oil In Water

Developing new therapeutic drugs to prevent ischemia/reperfusion (I/R)-induced renal injuries is highly pursued. Liposomal encapsulation of spironolactone (SP) as a mineralocorticoid antagonist increases dissolution rate, bioavailability and prevents the drug from degradation. In this context, this work develops a new formulation of oil-in-water type microemulsions to enhance the bioavailability of SP. The size of the SP-loaded microemulsion was about 6.0 nm by dynamic light scattering analysis. Briefly, we investigated the effects of nano-encapsulated SP (NESP) on renal oxidative stress, biochemical markers and histopathological changes in a rat model of renal I/R injury. Forty eight male Wistar rats were divided into six groups. Two groups served as control and injury model (I/R). Two groups received “conventional” SP administration (20 mg/kg) and NESP (20 mg/kg), respectively, for two days. The remaining two groups received SP (20 mg/kg) and NESP (20 mg/kg) two days before induction of I/R. At the end of the experiments, serum and kidneys of rats underwent biochemical, molecular and histological examinations. Our results showed that I/R induces renal oxidative stress, abnormal histological features and altered levels of renal biomarkers. Administration of SP in healthy animals did not cause any significant changes in the measured biochemical and histological parameters compared to the control group. However, SP administration in the I/R group caused some corrections in renal injury, although it could not completely restore I/R-induced renal oxidative stress and kidney damage. On the contrary, NESP administration restored kidney oxidative injury via decreasing renal lipid peroxidation and enhancing glutathione, superoxide dismutase and catalase in kidneys of the I/R group. The deviated serum levels of urea, creatinine, total proteins and uric acid were also normalized by NESP administration. Furthermore, NESP protected against renal abnormal histology features induced by I/R. Therefore, NESP has beneficial effects in preventing kidney damage and renal oxidative stress in a rat model of I/R, which deserves further evaluations in the future.

Intermedin protects against renal ischemia-reperfusion injury by inhibition of oxidative stress

2013 ◽  
Vol 304 (1) ◽  
pp. F112-F119 ◽  
Author(s):  
Xi Qiao ◽  
Rong-Shan Li ◽  
Hong Li ◽  
Guo-Zhen Zhu ◽  
Xiao-Guang Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Critical Role ◽  
Renal Ischemia ◽  
Kidney Cells ◽  
Sod Activity ◽  
Renal Ischemia Reperfusion Injury

Reactive oxygen species (ROS) play a critical role in renal ischemia-reperfusion injury (IRI). Intermedin (IMD) reportedly protected against myocardial IRI via its antioxidant effects; however, its protective role in renal IRI has not been investigated. We overexpressed IMD in rat kidneys and examined how the kidneys respond to renal IRI. Eukaryotic expression plasmid encoding the rat IMD gene or control empty vector was transfected into the left kidney using an ultrasound-microbubble-mediated delivery system. This method yielded high expression of IMD in kidney cells. Renal IRI was induced by clamping the left renal artery followed by reperfusion. In response to IRI, overexpression of IMD in the kidney significantly improved renal function and pathology compared with the kidney transfected with control plasmid. We investigated the mechanisms by which IMD protects against renal IRI. We examined renal superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and found SOD activity was significantly increased, while MDA level was markedly decreased in kidneys transfected with IMD, suggesting ROS production and oxidative stress were reduced by IMD overexpression. We also measured myeloperoxidase (MPO) activity, tubular cell apoptosis, and the expression of intercellular adhesion molecule-1 (ICAM-1), P-selectin, and endothelin-1 (ET-1) in the kidney. Renal MPO activity and the expression of ICAM-1, P-selectin, and ET-1 stimulated by IRI were significantly inhibited by IMD overexpression. Moreover, IMD overexpression prevented kidney cells from apoptosis caused by IRI. Our results demonstrate that overexpression of IMD in the kidney protects against renal IRI, apparently by reducing oxidative stress, consequently suppressing inflammation and vasoconstrictor production and apoptosis.

Study on the Protective Effect of Sevoflurane on H2O2-Induced HK-2 Cells

2019 ◽  
Vol 9 (5) ◽  
pp. 687-693 ◽  
Author(s):  
Cheng Guo ◽  
Jinyue Zhu ◽  
Shuang Wu ◽  
Xia Li ◽  
Ying Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Control Group ◽  
Renal Ischemia Reperfusion Injury ◽  
And Oxidative Stress

Background: Renal ischemia reperfusion injury (RIRI) is the main cause of acute kidney injury (AKI). The aim of this study was to investigate whether sevoflurane could protect HK-2 cells treated by H2O2 by improving apoptosis and oxidative stress through TLR4/MyD88/NF-κb signaling pathway. Methods: HK-2 cells was treated with H2O2 to construct the oxidative damage model happened in renal ischemia reperfusion injury (RIRI). CCK-8 assay was performed to analyze the viability of HK-2 cells. The reactive oxygen species (ROS), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdelyde (MDA) testing kits were used for the detection of oxidative stress related factors. TUNEL assay and Western blot were applied to analyze the apoptosis of HK-2 cells. And, proteins of TLR4/MyD88/NF-κb signaling pathway were also detected by western blot. Results: The viability of H2O2-induced HK-2 cells was decreased compared with the control group. The ROS, SOD and MDA levels were increased and LDH level was decreased in H2O2-induced HK-2 cells. The apoptosis of H2O2-induced HK-2 cells was increased. The expression of Bax was decreased and the expression of Bcl-2 and cleaved caspase 3 were increased in the H2O2-induced HK-2 cells. The expression of TLR4/MyD88/NF-κb signaling pathway was increased in the H2O2-induced HK-2 cells. All these changes were reversed by pretreatment with sevoflurane to some extent in HK-2 cells. Conclusion: In conclusion, sevoflurane pretreatment protects HK-2 cells treated by H2O2 by improving apoptosis and oxidative stress through inhibiting the TLR4/MyD88/NF-κb signaling pathway.

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