NADPH Oxidases in the Kidney

Gill, Pritmohinder; Wilcox, Christopher S.

doi:10.1089/ars.2006.8.1597

Cited by 436 publications

(419 citation statements)

References 76 publications

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“…Our results showed that G6PD activity, NADPH and GSH levels in the Cur group were higher than in the DC group. These results are similar to the previous descriptions [48][49][50][51][52].…”

Section: Discussionsupporting

confidence: 93%

Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

Xie

Zeng

et al. 2017

Open Life Sciences

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Abstract:We investigated the effect of curcumin on liver anti-oxidative stress in the type 1 diabetic rat model induced by streptozotocin (STZ). Experimental diabetic rats were induced by STZ intraperitoneally. All rats were fed for 21 days including three groups of control (NC), diabetic model (DC) and curcumin-treated (Cur, 1.5 g/kg by gavage). The results showed that curcumin-treatment significantly decreased the blood glucose and plasma malondialdehyde levels, but significantly increased the plasma superoxide dismutase, glutathione peroxidase and reduced glutathione levels. Curcumin treatment decreased the activity of aldose reductase, but increased the plasma glucose-6-phosphate dehydrogenase, glucose synthetase and glucose-polymerizing activities. Curcumin treatment significantly decreased the protein of protein kinase C (PKC) and poly ADP ribose polymerase (PARP) expression in the Cur group compared with the DC group. Moreover, the sorbitol dehydrogenase activity was significantly decreased and deterred glucose enters into the polyol pathway leading to an increased NADPH content in the Cur group compared with the DC group. Our data provides evidence that oxidative stress in diabetic rats may be attenuated by curcumin by inhibiting polyol pathway associated with down-regulated expression of PKC and PARP, as evidenced by both an increase the antioxidant enzymes levels and glycogen biosynthesis enzymes activities.

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“…Our results showed that G6PD activity, NADPH and GSH levels in the Cur group were higher than in the DC group. These results are similar to the previous descriptions [48][49][50][51][52].…”

Section: Discussionsupporting

confidence: 93%

Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

Xie

Zeng

et al. 2017

Open Life Sciences

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“…Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression that induces the production of reactive oxygen species, and triggers inflammatory response. [25][26][27][28] In this study, we found that aliskiren reduced oxidative stress and IL-6 expression in non-infarcted area similarly to valsartan with our tested doses. In addition, the combination of valsartan and aliskiren further suppressed oxidative stress and IL-6 expression in non-infarcted area than either monotherapy.…”

Section: Discussionsupporting

confidence: 60%

Aliskiren in combination with valsartan exerts synergistic protective effects against ventricular remodeling after myocardial infarction in mice

et al. 2011

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The efficacy of aliskiren, a direct renin inhibitor, in ventricular remodeling after myocardial infarction (MI) compared with conventional renin-angiotensin system (RAS) inhibitors remains to be defined. This study was performed to examine the protective effects of aliskiren and its addition to valsartan, an angiotensin-II receptor blocker, against ventricular remodeling after MI. MI was induced in 8-to 12-week-old C57BL/6 mice by ligating the left anterior descending artery. At 3 days after MI, mice were divided into five groups and were treated with the following: (1) phosphate-buffered saline (PBS); (2) hydralazine (10 mg kg -1 day -1 ); (3) valsartan (8 mg kg -1 day -1 ); (4) aliskiren (25 mg kg -1 day -1 ); and (5) combined aliskiren (25 mg kg -1 day -1 ) and valsartan (8 mg kg -1 day -1 ). With these doses of drugs, blood pressure-lowering effects compared with the PBS group were similar among the treated groups in sham-operated mice. At 28 days after MI, echocardiographic, hemodynamic and histological assessments demonstrated that monotherapy with valsartan or aliskiren alone significantly and similarly ameliorated ventricular remodeling after MI compared with the PBS and the hydralazine groups. Combination therapy of valsartan and aliskiren more greatly improved ventricular remodeling after MI with enhancement of angiogenesis and greater attenuation of tissue oxidative stress and inflammation. Our results indicate that aliskiren can be an alternative to conventional RAS inhibitors in the treatment of post-MI patients. Moreover, the dual therapy of valsartan and aliskiren may be more beneficial than either monotherapy. Further clinical trials will be warranted to sufficiently assess the safety and the efficacy of the use of aliskiren in post-MI patients.

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“…Increased oxidative stress in diabetic nephropathy could be attributed to an imbalance between ROS production and its removal capacity. Although multiple enzymatic pathways have been implicated in the generation of ROS in hyperglycaemia, NOX might be an important ROS source in diabetic kidney [32]. In particular, NOX-4 levels were shown to increase early in the STZ-induced diabetic rat model and NOX inhibition prevented diabetic changes of kidney [30,31,33].…”

Section: Discussionmentioning

confidence: 99%

Aggravation of diabetic nephropathy in BCL-2 interacting cell death suppressor (BIS)-haploinsufficient mice together with impaired induction of superoxide dismutase (SOD) activity

et al. 2013

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Aims/hypothesis B cell CLL/lymphoma 2 (BCL-2)-interacting cell death suppressor (BIS), known as an anti-stress and antiapoptotic protein, has been reported to modulate susceptibility to oxidative stress. This study investigated the potential role of BIS as an antioxidant protein in diabetic nephropathy. Methods Diabetes was induced in BIS-heterozygote (BIS-HT) mice via streptozotocin injections and the resulting phenotypes were compared with those of BIS-wild-type (BIS-WT) mice over the 20 weeks following diabetes induction.Results Renal injuries, represented by increased plasma creatinine levels and increased albuminuria, were greater in diabetic BIS-HT mice than in diabetic BIS-WT mice, and were accompanied by a significant increase in reactive oxygen species (ROS) and oxidative stress markers. Moreover, renal pathological changes and the apoptotic process were accelerated in diabetic BIS-HT mice compared with diabetic BIS-WT mice with the same degree of hyperglycaemia; all were restored by 4-hydroxy-2,2,6,6-tetramethylpiperidine-Noxyl (tempol) treatment. The levels of NADPH oxidase and related proteins were not significantly higher in diabetic BIS-HT mice compared with diabetic BIS-WT mice. However, levels of superoxide dismutase (SOD)1 and SOD2 increased on the induction of diabetes in BIS-WT mice but not in BIS-HT mice, correlating with the total SOD activity. An in vitro study showed that knockdown of BIS production also resulted in impaired induction of SOD activity as well as SOD levels in HK-2 and NMS cells, concomitant with significant ROS accumulation. Conclusion/interpretation Our results suggest that the decreased antioxidant capacity of BIS aggravates diabetic nephropathy in diabetic BIS-HT mice, possibly as a result of the disruption in the regulation of SOD protein quality under oxidative stress. Electronic supplementary material The online version of this article (doi:10.1007/s00125-013-3064-0) contains peer-reviewed but unedited supplementary material, which is available to authorised users.

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NADPH Oxidases in the Kidney

Cited by 436 publications

References 76 publications

Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

Aliskiren in combination with valsartan exerts synergistic protective effects against ventricular remodeling after myocardial infarction in mice

Aggravation of diabetic nephropathy in BCL-2 interacting cell death suppressor (BIS)-haploinsufficient mice together with impaired induction of superoxide dismutase (SOD) activity

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