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 Protective effect of cordycepin on experimental renal ischemia/reperfusion injury in rats

2020 ◽  
Vol 92 (4) ◽  
Author(s):  
Hasan Riza Aydin ◽  
Cagri Akin Sekerci ◽  
Ertugrul Yigit ◽  
Hatice Kucuk ◽  
Huseyin Kocakgol ◽  
...  
Keyword(s):  
Protective Effect ◽  
Rat Model ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Female Rat ◽  
Biochemical Analyses ◽  
The Right

Aim: To date, various molecules have been investigated to reduce the effect of renal ischemia/reperfusion (I/R) injury. However, none have yet led to clinical use. The present study aimed to investigate the protective effect of cordycepin (C) on renal I/R injury in an experimental rat model. Materials and methods: Twenty-four mature Sprague Dawley female rat was randomly divided into three groups: Sham, I/R, I/R+C. All animals underwent abdominal exploration. To induce I/R injury, an atraumatic vascular bulldog clamp was applied to the right renal pedicle for 60 minutes (ischemia) and later clamp was removed to allow reperfusion in all rats, except for the sham group. In the I/R + C group, 10 mg/kg C was administered intraperitoneally, immediately after reperfusion. After 4 hours of reperfusion, the experiment was terminated with right nephrectomy. Histological studies and biochemical analyses were performed on the right nephrectomy specimens. EGTI (endothelial, glomerular, tubulointerstitial) histopathology scoring and semi-quantitative analysis of renal cortical necrosis were used for histological analyses and superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), total oxidant status (TOS) for biochemical analyses. Results: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. The I/R group had higher histopathological scores than the I/R + C group. In the biochemical analysis of the tissues, SOD, MDA, TOS values were found to be statistically different in the I/R group compared to the I/R + C group (p: 0.004, 0.004, 0.001 respectively). Conclusions: Intraperitoneal cordycepin injection following ischemia preserve renal tissue against oxidative stress in a rat model of renal I/R injury.

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.

Abstract P298: Finerenone Protects Against the Acute and Chronic Consequences of Renal Ischemia/reperfusion Injury

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Jonatan Barrera-Chimal ◽  
Alan Le Mercier ◽  
Soumaya El-Moghrabi ◽  
Peter Kolkhof ◽  
Frederic Jaisser
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Kidney Injury ◽  
Fold Increase ◽  
Renal Ischemia ◽  
Mrna Levels ◽  
Beneficial Effects ◽  
The Right

Introduction: One of the most common causes of acute kidney injury (AKI) is renal ischemia/reperfusion (IR). Mineralocorticoid receptor (MR) antagonism has shown beneficial effects against renal IR consequences. The potential benefit of novel non-steroidal MR antagonists such as finerenone has not been explored. Objective: Evaluate the efficacy of finerenone to prevent the acute and chronic consequences of ischemic AKI. Methods: For the acute study (24 hours), 18 rats were divided in: sham, rats subjected to bilateral renal ischemia of 25 min and rats that received three doses of finerenone at -48 h, -24 h and -1 h before the ischemia. For the chronic study (4 months), 21 rats were divided in: sham, rats with 45 min of bilateral ischemia and rats treated with Finerenone at day -2, -1 and 1h before IR. The left kidney was used for histology and the right kidney for molecular analysis. Results: After 24 h of reperfusion, the untreated IR rats presented a 3-fold increase in plasma creatinine, accompanied by 40% of tubules presenting cell detachment and casts. Kim-1 and NGAL mRNA levels were induced by 30-fold. In contrast, the rats that received finerenone presented normal creatinine and significantly fewer injured tubules (11%) and a less pronounced induction of kim-1 and NGAL (8-fold). After 4 months, the untreated IR rats developed chronic kidney disease (CKD), evidenced by kidney dysfunction, increased proteinuria (121.6 vs. 14.3 mg/24h in sham) and renal vascular resistance (16.8 vs. 11.4 mmHg/mL in sham). Tubular dilation, extensive tubule-interstitial fibrosis and an increase in kidney TGF-β and Collagen-I mRNA levels also characterized CKD. The transition from AKI to CKD was fully prevented by finerenone administration at the time of IR. Conclusion: Altogether, our data shows that finerenone is able to prevent AKI induced by IR as well as the chronic and progressive deterioration of kidney function and structure.

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

2012 ◽  
Vol 27 (4) ◽  
pp. 340-345 ◽  
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.

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.

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

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Shady M Eldaif ◽  
Jeremiah Deneve ◽  
Ning Ping Wang ◽  
Mario Mosunjac ◽  
Rong Jiang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Arterial Occlusion ◽  
Control Group ◽  
Left Renal Artery ◽  
List Type ◽  
Protective Effects ◽  
Pkc Signaling

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.

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.

Which remote ischemic preconditioning protocol is favorable in renal ischemia-reperfusion injury in the rat?

2020 ◽  
Vol 76 (3) ◽  
pp. 439-451
Author(s):  
Gabor Varga ◽  
Souleiman Ghanem ◽  
Balazs Szabo ◽  
Kitti Nagy ◽  
Noemi Pal ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hematological Parameters ◽  
Renal Ischemia ◽  
Remote Ischemic Preconditioning ◽  
Optimal Timing ◽  
Delayed Effect ◽  
Artery Cannulation ◽  
The Right

BACKGROUND: The optimal timing of remote ischemic preconditioning (RIPC) in renal ischemia-reperfusion (I/R) injury is still unclear. We aimed to compare early- and delayed-effect RIPC with hematological, microcirculatory and histomorphological parameters. METHODS: In anesthetized male CrI:WI Control rats (n = 7) laparotomy and femoral artery cannulation were performed. In I/R group (n = 7) additionally a 45-minute unilateral renal ischemia with 120-minute reperfusion was induced. The right hind-limb was strangulated for 3×10 minutes (10-minute intermittent reperfusion) 1 hour (RIPC-1 group, n = 7) or 24 hour (RIPC-24 group, n = 6) prior to the I/R. Hemodynamic, hematological parameters and organs’ surface microcirculation were measured. RESULTS: Control and I/R group had the highest heart rate (p < 0.05 vs base), while the lowest mean arterial pressure (p < 0.05 vs RIPC-1) were found in the RIPC-24 group. The highest microcirculation values were measured in the I/R group (liver: p < 0.05 vs Control). The leukocyte count increased in I/R group (base: p < 0.05 vs Control), also this group’s histological score was the highest (p < 0.05 vs Control). The RIPC-24 group had a significantly lower score than the RIPC-1 (p = 0.0025 vs RIPC-1). CONCLUSION: Renal I/R caused significant functional and morphological, also in the RIPC groups. According to the histological examination the delayed-effect RIPC method was more effective.

Abstract 254: Ultrasound Improves the Outcomes After Cardiopulmonary Resuscitation by Stimulating the Cholinergic Anti-Inflammatory Pathway

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Peng Sun ◽  
Yuhan Zhang ◽  
Tingting Shu ◽  
Licai Liang ◽  
Weijing Shao ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hippocampal Neurons ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Mechanical Index ◽  
Inflammatory Pathway ◽  
The Us ◽  
Anti Inflammatory ◽  
The Right

Introduction: Recently it was shown that the ultrasound (US) treatment prevented renal ischemia- reperfusion injury (IRI) in mice. In the present study, we investigated the effects of the US treatment against IRI after CPR . Hypothesis: US would improve the outcomes after resuscitation in a rat model of CPR, and the protective effect of US would be dependent on the cholinergic anti-inflammatory pathway (CAP) via α7nAChR. Methods: The animals were randomized into 5 groups (n=8 each): (1) CPR group: the rats underwent 6 mins of untreated ventricular fibrillation (VF) followed by CPR and defibrillation; (2) US group: the treatment was identical to the CPR group except that rats were exposed to US treatment 24h before CPR; (3) MLA group: the treatment was identical to the US group except thatα7nAChR antagonist MLA (4mg/kg) was administered 30 mins prior to US treatment and VF respectively; (4) GTS group: the treatment was identical to the CPR group except that α7nAChR agonist GTS-21(4mg/kg) was injected 30 mins before VF. (5) SHAM group: the rats were exposed to surgical preparation without CPR and US application. One day before CPR, the US treatment was delivered to the left kidney by US pulses (contrast general mode with 9 MHz) with a bursting mechanical index of 0.72. US pulses were 1 second in duration and were applied once every 6 seconds for 2 mins. After the treatment of the left kidney, the right kidney was exposed to US treatment for another 2 mins. Results: Significantly longer duration of survival was observed in US-treated animals. And US treatment also suppressed the TNF-α and IL-6 following resuscitation, and improved neurological function. The expression of α7nAChR were promoted in hippocampal neurons in US group. Moreover, the protective effect of US treatment could be abolished by MLA and imitated by GTS-21. Conclusions: US treatment before IRI improves the outcomes after CPR, and CAP via α7nAChR plays an important role during CPR.

scholarly journals Curcumin Protects against Renal Ischemia/Reperfusion Injury by Regulating Oxidative Stress and Inflammatory Response

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xiaoying Cui ◽  
Lili Lin ◽  
Xiaoling Sun ◽  
Lin Wang ◽  
Rong Shen
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Renal Injury ◽  
Iron Reduction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Inflammatory Factors ◽  
Left Renal Artery ◽  
Contralateral Kidney

Objective. The aim of this study was to explore the pharmacological effects of curcumin on oxidative stress and inflammatory response of renal dysfunction induced by renal ischemia/reperfusion (RIRI). Methods. Fifty male SD rats (Sprague Dawley) were randomly divided into the sham group, RIRI group, and curcumin group (low, medium, and high). The RIRI model was established by clipping the left renal artery for 45 min and then reperfusion for 24 h and resection of the contralateral kidney. In the curcumin group, curcumin was intraperitoneally injected once a day for 3 consecutive days using different dosage regimens. The RIRI group was intraperitoneally administered with normal saline. Renal injury was evaluated by measuring the concentration of creatinine (Cr) and urea nitrogen (BUN) in serum. Oxidative stress was assessed by assessing the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), and iron reduction/antioxidant capacity (FRAP) in tissues. In addition, the protective effect of RIRI was investigated by measuring Paller scores, the level of serum inflammatory factors and caspase-3, and the number of apoptotic cells. Results. Ischemia/reperfusion resulted in increased levels of Cr and BUN in serum and MDA in tissues and decreased levels of SOD, CAT, GPx, GSH, and FRAP. Curcumin pretreatment strikingly increased the level of SOD, CAT, GPx, GSH, IL-10, IFN-γ, and FRAP and significantly decreased MDA, Cr, BUN, IL-8, TNF-α, IL-6, and myeloperoxidase (MPO) expressions in tissues. Conclusion. Curcumin can relieve the degree of renal injury and improve renal function in ischemia-reperfusion, which may be related to the fact that curcumin can increase SOD content in serum and reduce MDA and FRAP levels in the rat model.

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