NADPH Oxidases, Reactive Oxygen Species, and the Kidney

Sedeek, Mona; Nasrallah, Rania; Touyz, Rhian M.; Hébert, Richard

doi:10.1681/asn.2012111112

Cited by 391 publications

(322 citation statements)

References 49 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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“…Oxidative stress is associated with multiple factors that induce the development of CKD [16][17][18][19] , and eliminating oxidative stress is an alternative strategy for the treatment of CKD. In this study, we aimed to clarify the relationship between renal RAS activation and oxidative stress, and we investigated the effect of ROS elimination on RAS activation-induced renal fibrosis in the unilateral ureteral obstructive (UUO) model and on cultured renal fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

N-acetylcysteine alleviates angiotensin II-mediated renal fibrosis in mouse obstructed kidneys

Shen

Miao

et al. 2016

Acta Pharmacol Sin

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Aim: To investigate the effects of ROS scavenger N-acetylcysteine (NAC) on angiotensin II (Ang II)-mediated renal fibrosis in vivo and in vitro. Methods: Mice were subjected to unilateral ureteral obstruction (UUO), and then treated with vehicle or NAC (250 mg/kg, ip) for 7 days. Histological changes of the obstructed kidneys were observed with Masson's trichrome staining. ROS levels were detected with DHE staining. The expression of relevant proteins in the obstructed kidneys was assessed using Western blotting assays. Cultured rat renal fibroblast NRK-49F cells were used for in vitro experiments. Results: In the obstructed kidneys, Ang II levels were significantly elevated, and collagen I was accumulated in the interstitial spaces. Furthermore, ROS production and the expression of p47 (a key subunit of NADPH oxidase complexes) were increased in a timedependent manner; the expression of fibronectin, α-SMA and TGF-β were upregulated. Administration of NAC significantly alleviated the fibrotic responses in the obstructed kidneys. In cultured NRK-49F cells, treatment with Ang II (0.001-10 μmol/L) increased the expression of fibronectin, collagen I, α-SMA and TGF-β in dose-dependent and time-dependent manners. Ang II also increased ROS production and the phosphorylation of Smad3. Pretreatment with NAC (5 μmol/L) blocked Ang II-induced oxidative stress and ECM production in the cells. Conclusion: In mouse obstructed kidneys, the fibrotic responses result from Ang II upregulation can be alleviated by the ROS scavenger N-acetylcysteine.

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“…Previous studies indicated that high levels of UA promoted reactive oxygen species (ROS) generation to increase oxidative stress in several cell types, including mesangial cells, adipocytes and vascular smooth muscle cells (4)(5)(6). ROS are considered to be crucial mediators of cell apoptosis (7)(8)(9). In kidney disease, apoptosis is one of the main causes of tubular cell loss (10).…”

Section: Introductionmentioning

confidence: 99%

“…Nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) is the predominant Nox in the kidney (8,11). It generates ROS by transferring an electron to molecular oxygen.…”

Section: Introductionmentioning

confidence: 99%

“…It generates ROS by transferring an electron to molecular oxygen. Nox4-derived ROS have an important role in cell signaling as secondary messengers, mediating numerous biological processes, including cell apoptosis (7,8). However, it has remained elusive whether UA-mediated Nox4 expression represents an endogenous source of ROS in tubular cells.…”

Section: Introductionmentioning

confidence: 99%

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Nox4 has a crucial role in uric acid-induced oxidative stress and apoptosis in renal tubular cells

Sheng

Liu

et al. 2016

Molecular Medicine Reports

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Abstract. The purpose of the present study was to evaluate the effects of uric acid in promoting tubular cell apoptosis and verify the role of nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4)-induced oxidative stress in this process. HK-2 cells were used as a human proximal tubular cell model and co-cultured with various concentrations of uric acid with or without pre-treatment with the Nox4 inhibitor diphenylene iodonium (DPI). The apoptotic rate and the amount of reactive oxygen species (ROS) were examined by flow cytometry. Furthermore, levels of Nox4, phosphorylated (p)-P38, p-extracellular signal-regulated kinase (ERK), B-cell lymphoma 2 (Bcl-2) and Bcl-2-extra large (Bax) were detected by western blot analysis. The results showed that treatment with uric acid decreased HK-2 cell viability and promoted apoptosis in a dose-dependent manner. This was paralleled with an upregulation of Nox4 as well as ROS overproduction, which activated the phosphorylation of P38/ERK and caused an imbalance of Bax/Bcl-2 in HK-2 cells. Of note, inhibition of Nox4 with DPI prevented uric acid-induced cell injury by suppressing ROS generation and P38/ERK activation. In conclusion, it was demonstrated that elevated uric acid promoted ROS-induced tubular cell apoptosis by upregulating Nox4 expression. The present study therefore provided possible mechanisms and a potential therapeutic target of uric acid-induced chronic kidney disease.

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NADPH Oxidases, Reactive Oxygen Species, and the Kidney

Cited by 391 publications

References 49 publications

Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

N-acetylcysteine alleviates angiotensin II-mediated renal fibrosis in mouse obstructed kidneys

Nox4 has a crucial role in uric acid-induced oxidative stress and apoptosis in renal tubular cells

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