Renoprotective potency of amifostine in rat renal ischaemia-reperfusion

Chok, Mohammed Koussai; Conti, Marc; Almolki, Abdelhamid; Ferlicot, Sophie; Loric, Sylvain; Dürrbach, Antoine; Galand, Benoît; Droupy, S.; Eschwège, P.

doi:10.1093/ndt/gfq314

Cited by 15 publications

(7 citation statements)

References 28 publications

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“…The surgical technique was followed according to the method described by Choket al (18). Following anesthesia induced by intraperitoneal injection of xylazine (10 mg/kg bw) and ketamine (50 mg/kg bw), minimal laparotomy was made using minimal dissection.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Sodium hydrosulphide against renal ischemia/reperfusion and the possible contribution of nitric oxide in adult male Albino rats

Ibrahim¹,

Aziz²,

Kamel³

et al. 2015

BLL

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OBJECTIVES: This study evaluates the effects produced by H 2 S donor; sodium hydrosulfi de (NaHS), in a renal ischemia/reperfusion (IR) rat model and assesses the possible mediating role of nitric oxide (NO) in these H 2 S' effects. BACKGROUND: For several centuries, hydrogen sulfi de (H 2 S) had been known to be a highly toxic agent. Recent studies, however, indicated that apart from NO and CO, H 2 S is the third "gasotransmitter" involved in the regulation of various physiological functions. Nevertheless, its impact on renal IR injury remains unclear. METHODS: Rats were randomly divided into three groups: sham control; renal IR; and renal IR+NaHS groups. NaHS (100 μmol/kg, ip) was administered 30 min prior to the induction of renal ischemia. RESULTS: NaHS was found to attenuate signifi cantly the IR-induced elevations in the serum levels of urea, creatinine and tumor necrosis factor α (TNF-α) as compared with IR group. NaHS also signifi cantly compensated the defi cits in the total antioxidant capacities (TAC) and lowered the elevated malondialdehyde (MDA) levels observed with renal IR in renal, hepatic, pulmonary, and cardiac tissues. Furthermore, NaHS pretreatment down-regulated the renal IR-induced over-expression of inducible nitric oxide synthase (iNOS) and up-regulated the IR-induced suppression of endothelial nitric oxide synthase (eNOS). The loss of normal architecture, hemorrhage, and infl ammatory cells infi ltration detected by histopathological examination of renal, hepatic, pulmonary, and cardiac tissues in IR rats were markedly ameliorated by pre-ischemic NaHS treatment. CONCLUSION: NaHS protects against the effects of renal IR injury by acting primarily through a decrease in both pro-infl ammatory cytokines and iNOS expression as well as through up-regulation of the eNOS pathway. Furthermore, H 2 S has a powerful anti-oxidant and anti-apoptotic effects (Tab. 2, Fig. 6, Ref. 45). Text in PDF www.elis.sk. KEY WORDS:Hydrogen sulfi de, ischemia/reperfusion injury, nitric oxide, tumor necrosis factor α, malondialdehyde, total antioxidant capacities.

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Section: Surgical Proceduresmentioning

confidence: 99%

Sodium hydrosulphide against renal ischemia/reperfusion and the possible contribution of nitric oxide in adult male Albino rats

Ibrahim¹,

Aziz²,

Kamel³

et al. 2015

BLL

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“…[ 16 17 ] Although it was shown that some medicines are effective in preventing ischemia-reperfusion injury, we have very few data indicating the effects of amifostine in this regard. [ 14 18 ]…”

Section: Discussionmentioning

confidence: 99%

“…In this study, decrease in levels of MDA, increase in expression of cyclooxygenase-2 were detected in two groups that are treated with amifostine when compared with control group, but there was not any significant difference at GSH peroxidase and other antioxidant enzyme levels. [ 14 ]…”

Section: Discussionmentioning

confidence: 99%

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Protective effects of amifostine on ischemia-reperfusion injury of rat kidneys

et al. 2015

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Objectives:Amifostine is a drug which can eliminate free oxygen radicals that appear in the body after radiation or chemotherapeutic agent exposure. It is used to decrease the renal toxicity of cisplatin. The aim of this study was to determine the role of amifostine in warm ischemia kidney model for prevention of ischemia/reperfusion injury and also to find out the mechanism for prevention from ischemia/reperfusion injury if such an effect does exist.Materials and Methods:Adult female rats (n = 40) that used in our study were divided into three groups. Group 1: Control (n = 8), group 2: Ischemia-control (n = 16), group 3: Amifostine treated (n = 16). The effect of amifostine on ischemia/reperfusion injury investigated in rat kidneys.Results:At the 7th day, blood urea nitrogen level was statistically significantly higher in ischemia-control group than all groups (P = 0.001) and mean serum creatinine levels were found to be the highest in ischemia-control group (P = 0.091). Mean malondialdehyde levels in left kidneys removed on the 7th day were not significantly different (P = 0.105) at all three groups. Between ischemia-control group and amifostine group, there was a significant difference in reduced glutathione (GSH) levels (P = 0.001). In amifostine group, grade 4 necrosis was not detected neither on 7th day nor day 0.Conclusion:Amifostine could decrease the degree and severity of necrosis after reperfusion. Amifostine could not prevent membrane lipid peroxidation caused by superoxide anion radicals in kidney but they could protect tissues from the harmful effects of ischemia/reperfusion injury by increasing the level of reduced GSH which is a well-known oxygen radical eliminator.

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“…However, the side effects of NSAIDs, namely gastric irritation, peptic ulcer, renal failure, platelet inhibition and hemorrhage limit their use [9]. In previous studies too, amiphostin was reported to provide a renoprotective effect through inhibiting the COX-2 activity which increases in renal IR injury [37]. Senbel AM et al reported that the COX-2 selective antagonist celecoxib protected the kidney tissue from COX-2 activation-related oxidative injury [38].…”

Section: Discussionmentioning

confidence: 99%

The effect of etoricoxib on kidney ischemia–reperfusion injury in rats: A biochemical and immunohistochemical assessment

Albayrak

Kurt

Demirci

et al. 2014

International Immunopharmacology

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Renoprotective potency of amifostine in rat renal ischaemia-reperfusion

Abstract: Amifostine decreased the degree and severity of tubular damage after reperfusion, probably by scavenging oxygen free radicals and attenuating the cytotoxic effects of inflammatory infiltrates and apoptosis.

Cited by 15 publications

References 28 publications

Sodium hydrosulphide against renal ischemia/reperfusion and the possible contribution of nitric oxide in adult male Albino rats

Sodium hydrosulphide against renal ischemia/reperfusion and the possible contribution of nitric oxide in adult male Albino rats

Protective effects of amifostine on ischemia-reperfusion injury of rat kidneys

The effect of etoricoxib on kidney ischemia–reperfusion injury in rats: A biochemical and immunohistochemical assessment

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