Favorable balance of anti-oxidant/pro-oxidant systems and ablated oxidative stress in Brown Norway rats in renal ischemia-reperfusion injury

Nilakantan, Vani; Hilton, Gail; Maenpaa, Cheryl; Why, Scott K. Van; Pieper, Galen M.; Johnson, Christopher P.; Shames, Brian D.

doi:10.1007/s11010-007-9480-z

Cited by 26 publications

(31 citation statements)

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“…In our model, I/R injury significantly reduced Mn SOD and Cu/Zn SOD mRNA expression, resulting in increased superoxide, and caused oxidative stress. This corresponded well with previous reports that there is a loss of antioxidant proteins that contributes to overall oxidative stress in I/R injury (15,38). Treatment with MnTMPyP was insufficient to restore the expression of either of these two genes, indicating that this compound does not act by upregulation of antioxidant proteins.…”

Section: Discussionsupporting

confidence: 92%

“…Lucigenin-enhanced chemiluminescence was measured as previously described (24,38). Briefly, 10 M lucigenin was added to 0.5 ml of protein homogenate (100 mg/ml) in 50 mM Krebs-HEPES buffer, pH 7.4.…”

Section: Animal Model Of Renal I/r Injurymentioning

confidence: 99%

“…To determine whether the reported decrease in antioxidant proteins in I/R injury (15,38) was observed in our model and whether MnTMPyP was able to prevent damage to the kidney by upregulating these genes, we performed realtime quantitative PCR for mRNA levels of Mn SOD and Cu/Zn SOD in sham-operated and I/R-, vehicle-, and MnTMPyPtreated samples. There was a significant decrease in both Mn SOD and Cu/Zn SOD mRNA levels ( Fig.…”

Section: Effect Of Mntmpyp On Expression Of Omentioning

confidence: 99%

“…In vivo studies have shown that resistance to renal I/R injury is partly due to a decrease in oxidative stress and preservation of antioxidant proteins (5,38). Manganese superoxide dismutase (Mn SOD) and copper/zinc superoxide dismutase (Cu/Zn SOD) both protect against global cerebral ischemia by preventing early DNA fragmentation (17,18).…”

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confidence: 99%

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MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion

Liang¹,

Hilton²,

Mortensen³

et al. 2009

American Journal of Physiology-Renal Physiology

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, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion. Am J Physiol Renal Physiol 296: F266 -F276, 2009. First published December 17, 2008 doi:10.1152/ajprenal.90533.2008.-Oxidative stress and apoptosis are important factors in the etiology of renal ischemia-reperfusion (I/R) injury. The present study tested the hypothesis that the cell-permeant SOD mimetic manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP) protects the kidney from I/R-mediated oxidative stress and apoptosis in vivo. Male Sprague-Dawley rats (175-220 g) underwent renal I/R by bilateral clamping of the renal arteries for 45 min followed by reperfusion for 24 h. To examine the role of reactive oxygen species (ROS) in renal I/R injury, a subset of animals were treated with either saline vehicle (I/R Veh) or MnTMPyP (I/R Mn) (5 mg/kg ip) 30 min before and 6 h after surgery. MnTMPyP significantly attenuated the I/R-mediated increase in serum creatinine levels and decreased tubular epithelial cell damage following I/R. MnTMPyP also decreased TNF-␣ levels, gp 91phox , and lipid peroxidation after I/R. Furthermore, MnTMPyP inhibited the I/R-mediated increase in apoptosis and caspase-3 activation. Interestingly, although MnTMPyP did not increase expression of the antiapoptotic protein Bcl-2, it decreased the expression of the proapoptotic genes Bax and FasL. These results suggest that MnTMPyP is effective in reducing apoptosis associated with renal I/R injury and that multiple signaling mechanisms are involved in ROS-mediated cell death following renal I/R injury. acute ischemia-reperfusion; manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin; reactive oxygen species

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Section: Discussionsupporting

confidence: 92%

Section: Animal Model Of Renal I/r Injurymentioning

confidence: 99%

Section: Effect Of Mntmpyp On Expression Of Omentioning

confidence: 99%

mentioning

confidence: 99%

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MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion

Liang¹,

Hilton²,

Mortensen³

et al. 2009

American Journal of Physiology-Renal Physiology

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“…Brown Norway (BN) rats strain was discovered to be dramatically resistant to cardiac and renal I/R injury compared with other strains, while Sprague Dawley (SD) rats are more susceptible with I/R injury [9]. Resistance to the development of tubular damage after renal ischemia was also observed in BN rats, and higher levels of heat-shock proteins and ablated oxidative stress was believed to be the putative mechanism of this resistance [10,11].…”

Section: Introductionmentioning

confidence: 99%

Revealing the Underlying Mechanism of Ischemia Reperfusion Injury Using Bioinformatics Approach

Shen

Zhou

et al. 2013

Kidney Blood Press Res

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Background/Aims: To reveal the potential pathogenesis of ischemia/reperfusion (I/R) injury. Methods: GSE9943 were downloaded from Genome Expression Omnibus database, including I/R and control samples for both Brown Norway (BN) and Sprague Dawley (SD) rats (3 rats/each group). Then differentially expressed genes (DEGs) were identified by limma package. miRNA-target gene network pairs were predicted using WebGestalt, and protein-protein interactions (PPI) were identified based on STRING database, followed by the networks construction using Cytoscape. Next, ClusterONE was used for modules screening. Furthermore, functional analyses were performed to common DEGs and genes. Results: Totally, 23 common DEGs of BR and SD rats were screened, enriched in functions, such as regulation of cellular protein metabolic process, response to wounding, proteinaceous extracellular matrix, and Enzyme inhibitor activity. MIR-29A, MIR-29B and MIR-29C were discovered both in up- and down-regulated miRNA-target gene networks. Genes in the PPI network were significantly disturbed in p53 signaling, complement and coagulation cascades pathway. Four modules were found significantly disturbed cytochrome P450, Serine/threonine protein kinase, calcium binding and Transient receptor potential channel protein domains. Conclusion: During I/R injury, many genes mutated, interrupting several biological functions, pathways and protein domains. MIR-29C and TRPC6 were suggested to be potential novel targets for this disease.

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Clopidogrel protects from cell apoptosis and oxidative damage in a mouse model of renal ischaemia–reperfusion injury

Batteux

Chéreau

et al. 2011

The Journal of Pathology

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Renal ischaemia-reperfusion injury (IRI) is consecutive to tissue oxidative damage and cell apoptosis that lead to acute renal failure (ARF) in renal allografts. The aim of this study was to investigate the beneficial effects of a pretreatment by clopidogrel on renal IRI in mice. IRI was induced by bilateral renal ischaemia for 45 min followed by reperfusion. Sixty-two healthy male BALB/c mice were randomly assigned to one of the following groups: PBS + ischaemia-reperfusion (IR); clopidogrel + IR; PBS + sham IR; clopidogrel + sham IR. Clopidogrel (25 mg/kg) or PBS was administered per os to the animals via a gastric cannula 24 h before operation. All mice were given a single dose of clopidogrel or PBS. Renal function histological damage, renal cell apoptosis, renal antioxidant activities, and CD41 expression were determined 24 h after reperfusion. The survival rates were evaluated over 7 days. Animals pretreated with clopidogrel had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores, and improved survival rates following IR. Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression. Renal reduced glutathione, superoxide dismutase, and catalase activities were unmodified by the pretreatment with clopidogrel. However, clopidogrel resulted in an increased total antioxidant capacity of the kidney. Furthermore, pretreatment by clopidogrel decreased the number of CD41-positive cells. Thus, clopidogrel exerts protective effects on renal IRI in mice by abrogating renal cell apoptosis as a consequence of improved renal antioxidant capacity and could be tried as a novel therapeutic tool in renal IRI.

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Favorable balance of anti-oxidant/pro-oxidant systems and ablated oxidative stress in Brown Norway rats in renal ischemia-reperfusion injury

Cited by 26 publications

References 50 publications

MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion

MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion

Revealing the Underlying Mechanism of Ischemia Reperfusion Injury Using Bioinformatics Approach

Clopidogrel protects from cell apoptosis and oxidative damage in a mouse model of renal ischaemia–reperfusion injury

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