Effects of aminoguanidine against renal ischaemia–reperfusion injury in rats

Şahna, Engin; Parlakpınar, Hakan; Cihan, Ömer Faruk; Türköz, Yusuf; Acet, Ahmet

doi:10.1002/cbf.1196

Cited by 31 publications

(31 citation statements)

References 25 publications

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“…MDA is a stable metabolite of the free radical-mediated lipid peroxidation cascade and it is widely used as a marker of oxidative stress and lipid layer destruction. 42 In this study, although tissue MDA levels are clearly decreased by montelukast, its mechanism is not clear. Montelukast may directly eliminate free oxygen radicals or directly increase the antioxidant enzyme activity and prevent the inhibition of these enzymes.…”

Section: Discussioncontrasting

confidence: 54%

Beneficial Effects of Montelukast against Cisplatin-Induced Acute Renal Damage in Rats

et al. 2012

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Objective: In this study, the therapeutic and protective effects of montelukast against cisplatin (CP)-induced acute renal damage were investigated. Materials and Methods: Thirty-five female rats were divided into five groups as follows: (1) control, (2) montelukast (10 mg/kg daily for 10 days per-oral (p.o.), (3) CP (single dose 7 mg/kg intraperitoneally (i.p.)), (4) CP + montelukast (10 mg/kg daily for 10 days p.o., after 3 days of the injection of CP), (5) montelukast (10 mg/kg daily for 10 days p.o.) + CP (single dose 7 mg/kg i.p., after the last dose of montelukast). At the end of the experiment, malondialdehyde (MDA), a lipid peroxidation product, myeloperoxidase (MPO), and reduced glutathione (GSH) levels were determined in the renal tissue. Also, blood urea nitrogen (BUN) and creatinine (Cr) levels were assayed from the trunk blood samples. Results: CP treatment caused a significant elevation of MDA, MPO, BUN, and Cr levels when compared with the control group. Also, GSH levels were found to be reduced due to the CP treatment. Montelukast administration after CP injection ameliorated all of these parameters. Our histopathological findings (marked swelling of epithelial cells, tubular dilatation, tubular desquamation, and loss of brush border in the kidney) were consistent with the biochemical results. Conclusion: Montelukast treatment after CP injection exerted therapeutic effects against CP-induced acute kidney damage.

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Section: Discussioncontrasting

confidence: 54%

Beneficial Effects of Montelukast against Cisplatin-Induced Acute Renal Damage in Rats

et al. 2012

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“…These findings are in agreement with previous reports [25,29]. TBARS, a stable metabolite of the free radical mediated lipid peroxidation cascade, is widely used as a marker of oxidative stress and lipid layer destruction [30]. Elevated TBARS levels show that DOX causes oxidative stress and free radical formation in kidney tissue.…”

Section: Discussionsupporting

confidence: 93%

Protective effects of molsidomine against doxorubicin-induced renal damage in rats

Oğuz¹,

Beytur²,

Sarihan³

et al. 2016

CIM

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Purpose: The purpose of this study was to investigate the therapeutic and protective effects of molsidomine (MLS) against doxorubicin (DOX)-induced renal damage in rats.Methods: Forty rats were randomly divided into five groups (control, MLS, DOX, DOX+MLS and MLS+DOX groups). Thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO) and glutathione peroxidase (GPx) levels were determined from kidney tissues and blood urea nitrogen (BUN), creatinine (Cr) and albumin (Alb) levels also determined.Results: DOX treatment caused a significant increase in TBARS levels and a significant decrease in the GSH and CAT levels compared with the control group. In comparison, MLS administration before DOX injection caused a significant decrease in TBARS levels and also increases in GSH and CAT levels, whereas treatment of MLS after DOX injection did not show any beneficial effect on these parameters. All groups showed a significant increase in NO levels compared to the control group. There were no significant differences among the all groups for BUN and Cr levels. Serum level of Alb decreased in the DOX-treated groups when compared with control and MLS groups. The histopathological findings were in accordance with the biochemical results. MLS treatment reversed the DOX-induced kidney damage in group 4. MLS treatment before DOX injection exerted a protective effect against DOX-induced kidney damage.Conclusions: MLS shows promise as a possible therapeutic intervention for the prevention of kidney injury associated with DOX treatment. Additional studies are warranted.

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“…Serum Cr concentration is more significant than the BUN levels in the earlier phases of kidney disease. On the other hand, BUN begins to increase only after a marked renal parenchymal injury occurs [39] . These findings are compatible with the ischemic lesion related to the renal damage.…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependent Protective Effect of Ivabradine against Ischemia-Reperfusion-Induced Renal Injury in Rats

Beytur

Binbay²,

Sarıhan³

et al. 2011

Kidney Blood Press Res

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Background/Aims: This study was designed to investigate the dose-dependent protective effect of ivabradine, a specific inhibitor of the cardiac sinoatrial node, on renal ischemia-reperfusion (I/R) injury in rats. Methods: Rats were divided into six groups: group 1, control; group 2, I/R (60 min ischemia followed by 24 h reperfusion); groups 3 and 4, 0.6–6 mg/kg ivabradine; and groups 5 and 6, sham+0.6–6 mg/kg ivabradine. At the end of the study, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase contents were assayed in the kidney tissues; serum blood levels of urea nitrogen (BUN), creatinine (Cr) and albumin also were determined. Results: Tissue MDA levels were found to be significantly higher in the I/R group, whereas SOD and CAT levels were lower when compared to the control group. Ivabradine (0.6 mg/kg) treatment reduced the MDA levels and elevated the SOD and CAT enzyme activity. Treatment with a dose of 6 mg/kg ivabradine further increased MDA levels and did not ameliorate SOD or CAT activities. Serum levels of BUN and Cr were significantly higher in the I/R group. I/R+0.6 mg ivabradine reduced the elevated BUN and Cr levels. Conclusion: This study indicates that ivabradine exerts a dose-dependent response beyond heart rate reduction against renal I/R injury.

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Effects of aminoguanidine against renal ischaemia–reperfusion injury in rats

Cited by 31 publications

References 25 publications

Beneficial Effects of Montelukast against Cisplatin-Induced Acute Renal Damage in Rats

Beneficial Effects of Montelukast against Cisplatin-Induced Acute Renal Damage in Rats

Protective effects of molsidomine against doxorubicin-induced renal damage in rats

Dose-Dependent Protective Effect of Ivabradine against Ischemia-Reperfusion-Induced Renal Injury in Rats

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