Hesperidin Ameliorates Hepatic Ischemia-Reperfusion Injury in Sprague-Dawley Rats

ObjectiveHepatic ischemia and reperfusion (I/R) is a destructive event associated with high rates of liver failure after liver transplantation. Hesperidin significantly contributes to the antioxidant defense system and has been reported to act as a powerful agent against superoxide and hydroxyl radicals. Our objective was to investigate the protective effect of hesperidin against hepatic IR injury in a rat model.MethodsWe fed Sprague-Dawley rats either hesperidin (100 mg/kg/d) or saline. One week later, ischemia was induced by clamping the rats’ common hepatic artery and portal vein for 30 minutes. The rats were divided into 3 groups: 1. the sham operated group; 2. the I/R group; and 3. the I/R-hesperidin group.ResultsCompared to the sham group, the I/R group had higher expression of serum aspartate aminotransferase and serum alanine aminotransferase and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, nitric oxide, and albumin. Compared to the I/R group, the I/R-hesperidin group had higher expression of catalase, superoxide dismutase, antioxidant and nitric oxide and lower expression of serum aspartate aminotransferase and serum alanine aminotransferase.ConclusionsOur findings suggest that hesperidin is a potential therapeutic agent for hepatic I/R injury.     

Protective Effect of Citric Acid Against Hepatic Ischemia Reperfusion Injury in Sprague-Dawley Rats

ObjectiveHepatic ischemia reperfusion (I/R) injury is regarded as a serious concern in clinical practice. Citric acid reduces oxidative stress and inflammation during hypoxia and reoxygenation. Our objective was to investigate the protective effect of citric acid against hepatic I/R injury in rats.MethodsWe fed Sprague-Dawley rats either citric acid (100 mg/kg/d) or saline. One week later, ischemia was induced by clamping the rats’ common hepatic artery and portal vein for 30 minutes. The rats were randomly divided into 3 major groups that were treated as follows: 1. the sham operated group; 2. the I/R group; and 3. the I/R-citric acid group.ResultsCompared to the sham group, the I/R group had higher expression of aspartate aminotransferase and alanine aminotransferase and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, nitric oxide, and albumin. Compared to the I/R group, the I/R-citric acid group had higher expression of catalase, superoxide dismutase, antioxidants, and nitric oxide, and lower expression of aspartate aminotransferase and alanine aminotransferase.ConclusionsThese results suggest that citric acid therapy has significant therapeutic potential in ischemic liver injury.     

Effect of Seed of Cassia tora Extract in the Prevention of Remote Renal Reperfusion Injury

ObjectiveRenal ischemia/reperfusion (I/R) injury is characterized by the acute deterioration of renal function during ischemia and renal inflammation. Cassia tora has various effects, including antioxidant, antidiabetic, and hypolipidemic properties. In the present study, we investigated whether C tora has a renoprotective effect on I/R-induced acute kidney injury in rats.MethodsWe fed Sprague-Dawley rats either C tora (100 mg/kg/d) or saline. One week later, ischemia was induced by bilateral renal pedicle occlusion for 30 minutes, followed by reperfusion. Rats were randomized into 3 major groups, which were treated as follows: 1. the sham operation group; 2. the I/R group; and 3. the I/R-C tora group.ResultsCompared to the sham group, the I/R group had higher levels of blood urea nitrogen and serum creatinine in serum and lower expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, and nitric oxide. Compared to the I/R group, the I/R-C tora group had higher expression of catalase, superoxide dismutase, glutathione peroxidase, antioxidant, and nitric oxide, as well as lower levels of blood urea nitrogen and creatinine in serum.ConclusionsThese results suggest that C tora has significant therapeutic effects in ischemic renal injury.     

Protective effect of sitagliptin against renal ischemia reperfusion injury in rats

Abstract

This study was designed to investigate the protective effects of sitagliptin on renal damage induced by renal ischemia reperfusion (I/R) in rats. For this, rats were randomly divided into four groups (n?=?8): (1) sham group, in which the rats only underwent right nephrectomy; (2) right nephrectomy and left kidney ischemia (1?h) and reperfusion (24?h) group (I/R); (3) 5?mg/kg sitagliptin administrated group, per-oral once a day for two weeks; (4) 5?mg/kg sitagliptin administrated group, per-oral once a day for two weeks before left kidney I/R (n?=?8). Sitagliptin-treated rats that underwent renal I/R demonstrated significant decrease in the serum urea nitrogen and creatinine and also, lipid peroxidation, total oxidant status and malondialdehyde level in the renal tissue when compared to the renal I/R group. Additionally, reduced glutathione, glutathione peroxidase, superoxide dismutase, catalase and total antioxidative capacity were significantly increased after renal I/R in sitagliptin-treated rats. Our histopathological findings were in accordance with these biochemical results. In sum, in the current study all of our results indicated that sitagliptin treatment ameliorated renal damage induced by renal I/R in rats.     

Curcumin protects against ischemia/reperfusion injury in rat kidneys

OBJECTIVES: Renal ischemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allograft. We investigated the effect of curcumin on ischemia-reperfusion (I/R) injury and the antioxidant effects of curcumin in rats. METHODS: Thirty rats were randomly divided into five experimental groups (control, sham, curcumin, I/R and I/R+curcumin, n=6 each). Curcumin was administered (200 mg kg(-1)) orally to curcumin and I/R+curcumin groups for 7 days. Then, the rats were subjected to bilateral renal ischemia for 45 min and followed by reperfusion for 24 h. All rats were killed and kidney function tests, serum and tissue nitric oxide (NO), protein carbonyl (PC), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined. Histopathological examinations were also performed. RESULTS: Curcumin significantly improved the urea and cystatin C levels in I/R+curcumin group compared to I/R group (p<0.05). Reduction of serum GSH-Px was significantly improved by curcumin (p<0.001), but SOD enzyme activity did not alter (p>0.05). Treatment with curcumin also resulted in significant reduction in serum and tissue MDA, NO and PC and for tissue that were increased by renal I/R injury (p<0.001 for serum and p<0.05 for tissue, respectively). In histological examination, the rats treated with curcumin had nearly normal morphology of the kidney. CONCLUSIONS: Based on our results, it can be concluded that curcumin protects the kidneys against I/R injury via its antioxidant effects.     

Allicin Attenuates Myocardial Ischemia Reperfusion Injury in Rats by Inhibition of Inflammation and Oxidative Stress

ObjectiveTo explore the protective effect and underlying mechanism of allicin (ALC) on myocardial ischemia reperfusion (MI/R) injury in rats.MethodsThe model of MI/R injury in rats was induced by ligating the left anterior descending branch of the coronary artery. Thirty male Sprague-Dawley rats were randomly divided into 3 equal groups (n = 10): sham group, MI/R injury group, and ALC precondition group. Enzyme-linked immunosorbent assay was used to examine the expression of cardiac troponin I, CK-MB, interleukin-6, tumor necrosis factor-α, and interleukin-8 in the rats' serum. Hematoxylin and eosin staining was used to observe the myocardial pathologic morphology. A physiological recorder was used to measure cardiac systolic and diastolic function. Western blot analysis was used for detecting the expression of p38 and p-p38 in myocardium. The content of malondialdehyde and the activity of superoxide dismutase, catalase, and glutathione peroxidase in myocardium were examined by automatic analysis with the thiobarbituric acid chromogenic and dinitrobenzoic acid methods, respectively.ResultsALC can significantly decrease the expression of cardiac troponin I, CK-MB, interleukin-6, tumor necrosis factor-α, and interleukin-8 in the serum and reduce the myocardial pathologic injury and the expression of malondialdehyde and p-p38 in myocardial tissue. Moreover, ALC can upregulate the activity of superoxide dismutase, catalase, and glutathione peroxidase and improve myocardial systolic and diastolic function with no influence on the expression of p38.ConclusionALC can protect rats against MI/R injury by suppressing inflammation and oxidative stress. The mechanism is associated with alleviating the activation of p38 signaling.     

Rutin attenuates gentamicin-induced renal damage by reducing oxidative stress,inflammation, apoptosis,and autophagy in rats

Abstract

Gentamicin is commonly used against gram-negative microorganisms. Its therapeutic use is mainly limited by nephrotoxicity. This study was aimed at evaluating the effect of rutin on oxidative stress, inflammation, apoptosis, and autophagy in gentamicin-induced nephrotoxicity in rats. The rats were treated with saline intraperitoneally (group I), 150?mg/kg of rutin orally (group II), 80?mg/kg of gentamicin intraperitoneally for 8?d (group III), or 150?mg/kg of rutin plus 80?mg/kg of gentamicin (group IV). The serum urea, creatinine, kidney malondialdehyde (MDA), and reduced glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity and protein concentration were measured, and renal histopathology analysis and immunohistochemical staining were performed. Rutin pretreatment attenuated nephrotoxicity induced by gentamicin by reducing the urea, creatinine, and MDA levels and increasing the SOD, CAT, and GPx activity, and the GSH levels. The rutin also inhibited inducible nitric oxide synthase (iNOS), cleaved caspase-3 and light chain 3B (LC3B), as evidenced by immunohistochemical staining. The present study demonstrates that rutin exhibits antioxidant, anti-inflammatory, anti-apoptotic, and anti-autophagic effects and that it attenuates gentamicin-induced nephrotoxicity in rats.     

Beneficial Effects of N-Acetylcysteine and Ebselen on Renal Ischemia/Reperfusion Injury

Abstract

Introduction: It has been demonstrated that peroxynitrite accompanies acute renal ischemia and contributes to the pathophysiology of renal damage. Therefore, we aimed to investigate the roles of N-acetylcysteine (NAC), a well-known powerful antioxidant, and ebselen (E), a scavenger of peroxynitrite, on renal injury induced by renal ischemia/reperfusion injury (IRI) of rat kidney. Materials and methods: Forty male Sprague–Dawley rats were divided into five groups: sham, renal IRI, renal IRI+NAC, renal IRI+E, and renal IRI+NAC+E. IR injury was induced by 60 min of bilateral renal ischemia followed by 6 h of reperfusion. After reperfusion, kidneys and blood samples were obtained for histopathological and biochemical evaluations. Results: Renal IR resulted in increased malondialdehyde and nitrite/nitrate levels suggesting increased lipid peroxidation and peroxynitrite production and decreased superoxide dismutase and glutathione peroxidase activities. Both NAC and E alone significantly decreased malondialdehyde and nitrite/nitrate levels and increased superoxide dismutase and glutathione peroxidase activities. Additionally in the renal IRI+NAC+E group, all biochemical results were quite close to those of sham group. Histopathologically, the kidney injury in rats treated with combination of NAC and E was found significantly less than the other groups. Conclusions: Both NAC and E are able to ameliorate IRI of the kidney by decreasing oxidative and nitrosative stresses and increasing free radical scavenger properties. Additionally, combination of NAC and E prevents kidney damage more than when each drug is used alone, suggesting that scavenging peroxynitrite nearby antioxidant activity is important in preventing renal IRI.     

Antioxidant enzyme gene expression in rats with remnant kidney induced chronic renal failure

Reactive oxygen intermediates play a role in chronic renal injury and glomerulosclerosis. We investigate changes in renal cortex antioxidant enzyme gene expression in the rat remnant-kidney model of chronic renal failure and compare the new data to enzyme activities published earlier. Antioxidant enzyme gene expression is evaluated by Northern blot analysis of cortex mRNA, using cDNA probes for catalase, copper/zinc-containing superoxide dismutase, and glutathione peroxidase. Catalase gene expression decreases during development of renal failure; this decrease is accompanied by decreased catalase activity during the glomerulosclerosis phase of the remnant-kidney model. Copper/zinc superoxide dismutase and glutathione peroxidase gene expression remain at a normal level during progression of the model, whereas their activities show a temporary decrease in the early remnant kidney. In the remnant-kidney model, catalase seems to be more vulnerable to reactive oxygen intermediates than superoxide dismutase and glutathione peroxidase. Our results show that antioxidant enzyme activity and gene expression do not change in the same direction at all times during disease development and that all antioxidant enzymes do not respond in the same way.     

Polyenylphosphatidylcholine pretreatment ameliorates ischemic acute renal injury in rats

AIM: Polyenylphosphatidycholine has been demonstrated to have antioxidant, cytoprotective and anti-inflammatory effects. Whether polyenylphosphatidycholine pretreatment affects ischemia/reperfusion-induced renal damage in vivo is not known and was investigated here in rats. METHODS: Forty female Sprague-Dawley rats were divided into three groups. Group 1 (n = 10) was given saline (control, sham operated). Group 2 (n = 15) were given saline, and Group 3 (n = 15) were given polyenylphosphatidycholine (100 mg/day for 10 days prior to experiment). Groups 2 and 3 were subjected to bilateral renal ischemia (60 min) followed by reperfusion (6 h). After the reperfusion period, the rats were sacrificed and kidney tissue superoxide dismutase, glutathione, total nitrite and nitrate, malondialdehyde and myeloperoxidase levels, plasma aspartate aminotransferase, blood urea nitrogen and creatinine concentrations, and nuclear factor kappa beta expression were determined. RESULTS: Serum levels of aspartate aminotransferase, blood urea nitrogen and creatinine were significantly decreased (P < 0.05) in the treatment group compared to those in the ischemic group. There were significant differences between treatment and ischemic groups regarding the tissue superoxide dismutase, glutathione, total nitrite and nitrate, malondialdehyde, and myeloperoxidase levels (P < 0.05). In addition, polyenylphosphatidycholine pretreatment reduced nuclear factor kappa beta expression in ischemic kidney tissue. Kidneys obtained from rats pretreated with polyenylphosphatidycholine demonstrated marked reduction of the histological features of renal injury compared to kidneys obtained from Group 2 rats, including a little vacuolization, pyknosis and necrosis. CONCLUSIONS: Polyenylphosphatidycholine pretreatment provided significant protection against ischemia/reperfusion injury to the kidney. This treatment could be therapeutic in kidney transplantation and other conditions associated with ischemia/reperfusion injury to the kidney.     

Nigella sativa protects against ischaemia/reperfusion injury in rat kidneys.

BACKGROUND: Renal ischaemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allografts, which is a complex pathophysiologic process involving hypoxia and free radical (FR) damage. The oil of Nigella sativa (NSO) has been subjected to considerable pharmacological investigations that have revealed its antioxidant activity in different conditions. But there is no previously reported study about its effect on ischaemia/reperfusion (I/R) injury of kidneys. The aim of this study was to investigate the possible effects of NSO in I/R-induced renal injury in rats. METHODS: Thirty healthy male Wistar albino rats were randomly assigned to one of the following groups: control, sham, I/R, NSO+I/R, I/R+NSO and NSO. I/R, NSO+I/R and I/R+NSO rats were subjected to bilateral renal ischaemia followed by reperfusion and then all the rats were killed and kidney function tests, serum and tissue oxidants and antioxidants were determined and histopathological examinations were performed. RESULTS: Pre- and post-treatment with NSO produced reduction in serum levels of blood urea nitrogen (BUN) and creatinine caused by I/R and significantly improved serum enzymatic activities of superoxide dismutase (SOD) and glutathion peroxidase (GSH-Px) and also tissue enzymatic activities of catalase (CAT), SOD and GSH-Px. NSO treatment resulted in lower total oxidant status (TOS) and higher total antioxidant capacity (TAC) levels and also significant reduction in serum and tissue malondialdehyde (MDA), nitric oxide (NO) and protein carbonyl content (PCC) that were increased by renal I/R injury. The kidneys of untreated ischaemic rats had a higher histopathological score, while treatment with NSO nearly preserved the normal morphology of the kidney. CONCLUSIONS: In view of previous observations and our data, with the potent FR scavenger and antioxidant properties, NSO seems to be a highly promising agent for protecting tissues from oxidative damage and preventing organ damage due to renal I/R.     

Effects of polyhemoglobin-antioxidant enzyme complex on ischemia-reperfusion in kidney

INTRODUCTION: The kidney suffers ischemia-reperfusion (I/R) injury during transplantation. The purpose of the present study was to investigate the therapeutic effect of artificials cells on renal I/R injury through biochemical assays and histological examination. METHODS: We prepared artificial cells using cross-linked hemoglobin (Hb), superoxide dismutase (SOD), and catalase. Normal male Sprague-Dawley rats were divided into 6 groups: the sham-operated control group, the group treated with polyHb,and the group treated with polyHb-SOD-catalase (PSC) (per groups were subjected to ischemia for 1 hour or 2 hours). After reperfusion for 4 hours, kidney and blood samples were obtained. RESULTS: The levels of SOD and catalase in the PSC group were 15 and 50 times higher than those of the control group, respectively. In the polyHb group, the levels of blood urea nitrogen (BUN), serum creatinine, renal hydrogen peroxide, and renal malondialdehyde were increased. However, their levels were significantly decreased by PSC administration. Renal SOD activity did not show any significant changes in the polyHb group, but renal catalase activity was decreased by polyHb treatment in comparison with the control group. The activities of renal SOD and catalase were increased using PSC treatment. In the histological findings, the PSC group showed no evidence of acute tubular necrosis in proximal convoluted tubules; their microvilli and cytoplasmic microorganelles were relatively well preserved. CONCLUSIONS: These results show that PSC effectively reduces renal damage via diminished oxygen free radical-mediated injury after I/R.     

NF-κB and COX-2 repression with topical application of hesperidin and naringin hydrogels augments repair and regeneration of deep dermal wounds

IntroductionWound injury is common and causes serious complications if not treated properly. The moist dressing heals wounds faster than other dressings. Therefore, we sought to study the effect of hesperidin/naringin hydrogel wound dressing or their combinations on the deep dermal wounds in mice.MethodsA rectangular full thickness skin flap of 2.5 × 1.5 cm was excised from depilated mice dorsum and the wound was fully covered with 5% hesperidin/5% naringin hydrogel or both in the ratio of 1:1, 2:1, or 1:2, respectively once daily until complete healing of the wound. Data were collected on wound contraction, mean wound healing time, collagen, DNA, and nitric oxide syntheses, glutathione concentration, superoxide dismutase activity, and lipid peroxidation throughout healing. Expression of NF-κB and COX-2 were also estimated in the regenerating granulation tissue using Western blot.FindingsDressing of wounds with 5% hesperidin hydrogel led to a higher and early wound contraction and significantly reduced mean wound healing time by 5.7 days than 5% naringin or combination of hesperidin and naringin hydrogels in the ratio of 1:1, 2:1, or 1:2. Hesperidin hydrogel wound dressing caused higher collagen and DNA syntheses than other groups at all times after injury. Glutathione concentration and superoxide dismutase activity increased followed by a decline in lipid peroxidation in regenerating wounds after hesperidin/naringin hydrogel application and a maximum effect was observed for hesperidin alone. The hesperidin/naringin hydrogel suppressed NF-κB and COX-2 expression on days 6 and 12.ConclusionsApplication of 5% hesperidin hydrogel was more effective than 5% naringin or combination of hesperidin and naringin gels (1:1, 2:1 or 1:2) indicated by a greater wound contraction, reduced mean wound healing time, elevated collagen and DNA syntheses, rise in glutathione concentration, and superoxide dismutase activity followed by reduced lipid peroxidation, and NF-κB, and COX-2 expression.     

Protective Effect of Alpha 1-Antitrypsin on Renal Ischemia-Reperfusion Injury

Backgroundα₁-Antitrypsin (AAT) is an important protein in the anti-inflammatory response that functions to regulate the activity of serine proteinases. We aimed to evaluate the protective effect of AAT on ischemia-reperfusion injury (IRI) in a mouse model.MethodsWe investigated the effects of AAT in a C57BL/6 mouse model of IRI by dividing them into 4 groups: normal control, sham operated, ischemia-reperfusion (IR), and IR after AAT pretreatment (IR-AAT). In the IR-AAT group, mice were pretreated with AAT (80 mg/kg/d) for 3 days before renal ischemia was induced by clamping the bilateral renal vascular pedicles for 30 minutes. At 24 hours after IRI, biochemistry, histology, inflammatory cytokines, and apoptosis were assayed.ResultsBlood urea nitrogen and serum creatinine levels were significantly lower in the IR-AAT group than in the IR group. Neutrophil gelatinase-associated lipocalin and kidney injury molecule 1 protein levels were significantly lower in the IR-AAT group than in the IR group. In addition, there were fewer tubular injuries and less interstitial fibrosis in the IR-AAT group than in the IR group, and the expression levels of transforming growth factor β, interleukin 1β, and interleukin 6 were significantly lower in the IR-AAT group than in the IR group. When compared with the IR group, there were fewer terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay–positive cells, lower caspase 3 activity and B-cell lymphoma 2-associated X protein (Bax), and higher B-cell lymphoma 2 (Bcl–2) in the IR-AAT group.Conclusionsα₁-Antitrypsin preserved renal function, attenuated tubular injuries and interstitial fibrosis, and inhibited inflammation and apoptosis after renal IRI. Our results suggest that AAT has protective effects against renal IRI by inhibiting inflammatory and apoptosis pathways.     

Antioxidant and protective effects of silymarin on ischemia and reperfusion injury in the kidney tissues of rats

Background Renal ischemia/reperfusion (I/R) injury is a major cause of acute renal failure. Silymarin is extracted from Silybum marianum and Cynara cardunculus seeds and fruits. The aim of this study is to investigate whether silymarin administration prevents the damage induced by I/R in rat kidneys. Materials and methods Thirty male Wistar rats were randomly divided into five experimental groups (n = 6, each) as follows; control group, sham-operated group, I/R group, silymarin group, and I/R + silymarin group. In the I/R and I/R + silymarin groups, both renal arteries were occluded using nontraumatic microvascular clamps for 45 min. Then, at the end of 24 h of reperfusion, the animals were killed. Kidney function tests, the serum and tissue antioxidant enzymes and oxidant products were determined. Results Animals that were subjected to I/R exhibited significant increase in serum urea, creatinine, and cystatin C levels compared with the rats treated with silymarin prior to the I/R process (P < 0.001). The serum enzymatic activities of superoxide dismutase and glutathione peroxidase significantly decreased in the I/R group; however, this reduction was significantly improved by the treatment with silymarin (P < 0.001 and P < 0.05, respectively). Renal I/R produced a significant increase in serum and tissue malondialdehyde, nitric oxide, and protein carbonyl as compared with controls. Treatment with silymarin resulted in significant reduction in these markers (P < 0.001). Conclusion Based on our findings, silymarin protects the kidneys against I/R injury. This finding may provide a basis for the development of novel therapeutic strategies for protection against the damages caused by I/R.     

Renoprotective effect of Spirulina fusiformis on cisplatin-induced oxidative stress and renal dysfunction in rats

Cisplatin is an effective chemotherapeutic agent used in the treatment of a wide array of both pediatric and adult malignancies. Dose-dependent and cumulative nephrotoxicity is the major toxicity of this compound, sometimes requiring a reduction in dose or discontinuation of treatment. Recent evidences have implicated oxidative and nitrosative stress in cisplatin-induced nephrotoxicity. Spirulina fusiformis, blue-green algae, is claimed to be a potential antioxidant. The present study was designed to explore the renoprotective potential of Spirulina fusiformis against cisplatin-induced oxidative stress and renal dysfunction. Spirulina fusiformis (500,1000,1500 mg/kg(-1) p.o.) was administered 2 days before and until 3 days after cisplatin challenge (5 mg/kg(-1) i.p.). Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine and urea clearance, and serum nitrite levels. Renal oxidative stress was determined by renal TBARS levels, reduced glutathione levels, and by enzymatic activity of superoxide dismutase and catalase. A single dose of cisplatin produced marked renal oxidative and nitrosative stress and significantly deranged renal functions. Chronic Spirulina fusiformis treatment significantly and dose-dependently restored renal functions, reduced lipid peroxidation, and enhanced reduced glutathione levels, superoxide dismutase, and catalase activities. The results of the present study clearly demonstrate the pivotal role of reactive oxygen species and their relation to renal dysfunction and point to the therapeutic potential of Spirulina fusiformis in cisplatin-induced nephrotoxicity.     

The Effect of Dietary Ginger (Zingiber officinals Rosc) on Renal Ischemia/Reperfusion Injury in Rat Kidneys

Oxidative stress has been considered as one of the possible mechanisms of ischemia/ reperfusion (I/R) injury in the kidney. The aim of this study was to analyze the possible protective effect of dietary ginger (Zingiber officinals Rosc), a free radical scavenger, on renal I/R injury in rats. The protective effect of ginger against the damage inflicted by reactive oxygen species (ROS) during renal I/R was investigated in Wistar albino rats using histopathological and biochemical parameters. Thirty rats were randomly divided into five experimental groups (i.e., control, sham-operated, ginger, I/R, and I/R + ginger groups, n = 6 each). The ginger and I/R + ginger groups were fed on the test diet containing 5% ginger. The rats were subjected to bilateral renal ischemia followed by reperfusion in I/R and I/R + ginger groups. At the end of the reperfusion period, rats were sacrificed, and kidney function tests, serum and tissue oxidants and antioxidants, and renal morphology were evaluated. Serum urea, creatinine, and cystatin C (CYC) levels were significantly elevated in the ischemia group, but these levels remained unchanged in the ginger + I/R group compared to the I/R group. Reduction of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) enzyme activity was significantly improved by the treatment with ginger compared to I/R group. Administration of ginger resulted in significant reduction levels of tissue malondialdehyde (MDA), NO, protein carbonyl contents (PCC) in the ginger + I/R group compared with the I/R group. Ginger supplementation in the diet before I/R injury resulted in higher total antioxidant capacity (TAC) and lower total oxidant status (TOS) levels than I/R group. The ginger supplemented diet prior to I/R process demonstrated marked reduction of the histological features of renal injury. The findings imply that ROS play a causal role in I/R-induced renal injury, and ginger exerts renoprotective effects probably by the radical scavenging and antioxidant activities.     

Renoprotective Effect of Spirulina fusiformis on Cisplatin-Induced Oxidative Stress and Renal Dysfunction in Rats

Cisplatin is an effective chemotherapeutic agent used in the treatment of a wide array of both pediatric and adult malignancies. Dose-dependent and cumulative nephrotoxicity is the major toxicity of this compound, sometimes requiring a reduction in dose or discontinuation of treatment. Recent evidences have implicated oxidative and nitrosative stress in cisplatin-induced nephrotoxicity. Spirulina fusiformis, blue-green algae, is claimed to be a potential antioxidant. The present study was designed to explore the renoprotective potential of Spirulina fusiformis against cisplatin-induced oxidative stress and renal dysfunction. Spirulina fusiformis (500,1000,1500 mg/kg^?1 p.o.) was administered 2 days before and until 3 days after cisplatin challenge (5 mg/kg^?1 i.p.). Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine and urea clearance, and serum nitrite levels. Renal oxidative stress was determined by renal TBARS levels, reduced glutathione levels, and by enzymatic activity of superoxide dismutase and catalase. A single dose of cisplatin produced marked renal oxidative and nitrosative stress and significantly deranged renal functions. Chronic Spirulina fusiformis treatment significantly and dose-dependently restored renal functions, reduced lipid peroxidation, and enhanced reduced glutathione levels, superoxide dismutase, and catalase activities. The results of the present study clearly demonstrate the pivotal role of reactive oxygen species and their relation to renal dysfunction and point to the therapeutic potential of Spirulina fusiformis in cisplatin-induced nephrotoxicity.     

Evaluation of Renoprotective Effect of Aphanizomenon flos-aquae on Cisplatin-Induced Renal Dysfunction in Rats

Cisplatin is an effective chemotherapeutic agent used in the treatment of a wide array of both pediatric and adult malignancies. Dose-dependent and cumulative nephrotoxicity is the major toxicity of this compound, sometimes requiring a reduction in dose or discontinuation of treatment. Recent evidence has implicated oxidative and nitrosative stress in cisplatin-induced nephrotoxicity. Aphanizomenon flos-aquae (AFA), blue-green algae, is claimed to be a potential antioxidant. The present study was designed to explore the renoprotective potential of AFA against cisplatin-induced oxidative stress and renal dysfunction. The ethanolic extract of Aphanizomenon flos-aquae (EEAFA) (25, 50, 100 mg/kg^?1 p.o.) was administered two days before through three days after cisplatin challenge (5 mg/kg^?1 i.p.). Renal injury was assessed by measuring serum creatinine, blood urea nitrogen, creatinine and urea clearance, and serum nitrite levels. Renal oxidative stress was determined by renal TBARS levels, reduced glutathione levels, and enzymatic activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione transferase (GST). A single dose of cisplatin produced marked renal oxidative and nitrosative stress and significantly deranged renal functions. Chronic EEAFA treatment significantly and dose-dependently restored renal functions, reduced lipid peroxidation, and enhanced reduced glutathione levels, superoxide dismutase, and catalase activities. The results of the present study clearly demonstrate the pivotal role of reactive oxygen species and their relation to renal dysfunction and point to the therapeutic potential of AFA in cisplatin-induced nephrotoxicity.