Oxidative Stress and Hypoxia in the Pathogenesis of Diabetic Nephropathy

Palm, Fredrik; Nordquist, Lina; Wilcox, Christopher S.; Hansell, Peter

doi:10.1007/978-1-60761-857-7_29

Cited by 9 publications

(13 citation statements)

References 224 publications

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“…ROS generation (O 2 − , H 2 O 2 , and OH − ) [ 28 ] is extraordinarily attentive because they are harmful to almost every organs and exacerbate both aging and disease processes. The production of ROS in DM and DN is mainly due to the enhanced activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and increased mitochondrial superoxide [ 29 ]. ROS have no specific target for action.…”

Section: Pathophysiologic Changes Of Ci-aki In Kidney Under Hgsmentioning

confidence: 99%

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Kawaguchi

2020

Contrast Media & Molecular Imaging

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Contrast-induced acute kidney injury (CI-AKI) is the third most common hospital-acquired AKI after AKI induced by renal perfusion insufficiency and nephrotoxic drugs, taking great adverse effects on the prognosis and increasing hospital stay and medical cost. Diabetes nephropathy (DN) is a common chronic complication of DM (diabetes mellitus), and DN is an independent risk factor for chronic kidney disease (CKD) and CI-AKI. The incidence of CI-AKI significantly increases in patients with renal injury, especially in DM-related nephropathy. The etiology of CI-AKI is not fully clear, and research studies on how DM becomes a facilitated factor of CI-AKI are limited. This review describes the mechanism from three aspects. ① Pathophysiological changes of CI-AKI in kidney under high-glucose status (HGS). HGS can enhance the oxidative stress and increase ROS which next causes stronger vessel constriction and insufficient oxygen supply in kidney via vasoactive substances. HGS also aggravates some ion pump load and the latter increases oxygen consumption. CI-AKI and HGS are mutually causal, making the kidney function continue to decline. ② Immunological changes of DM promoting CI-AKI. Some innate immune cells and pattern recognition receptors (PRRs) in DM and/or DN may respond to some damage-associated molecular patterns (DAMPs) formed by CI-AKI. These effects overlap with some pathophysiological changes in hyperglycemia. ③ Signaling pathways related to both CI-AKI and DM. These pathways involved in CI-AKI are closely associated with apoptosis, inflammation, and ROS production, and some studies suggest that these pathways may be potential targets for alleviating CI-AKI. In conclusion, the pathogenesis of CI-AKI and the mechanism of DM as a predisposing factor for CI-AKI, especially signaling pathways, need further investigation to provide new clinical approaches to prevent and treat CI-AKI.

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Section: Pathophysiologic Changes Of Ci-aki In Kidney Under Hgsmentioning

confidence: 99%

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Kawaguchi

2020

Contrast Media & Molecular Imaging

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“…Importantly, increased oxidative stress is intimately linked to the development of diabetic nephropathy (38). All strains displayed a close relationship between oxidative stress, measured as urinary excretion of TBARS, and proteinuria, and it was the two strains presented with the highest levels of oxidative stress, BALB/c and 129Sv, that also developed the most pronounced proteinuria in the present study.…”

Section: Discussionmentioning

confidence: 89%

Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes

Franzén

Friederich‐Persson

Fasching

et al. 2014

American Journal of Physiology-Renal Physiology

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One-third of diabetes mellitus patients develop diabetic nephropathy, and with underlying mechanisms unknown it is imperative that diabetic animal models resemble human disease. The present study investigated the susceptibility to develop diabetic nephropathy in four commonly used and commercially available mouse strains with type 1 diabetes to determine the suitability of each strain. Type 1 diabetes was induced in C57Bl/6, NMRI, BALB/c, and 129Sv mice by alloxan, and conscious glomerular filtration rate, proteinuria, and oxidative stress levels were measured in control and diabetic animals at baseline and after 5 and 10 wk. Histological alterations were analyzed using periodic acid-Schiff staining. Diabetic C57Bl/6 displayed increased glomerular filtration rate, i.e., hyperfiltration, whereas all other parameters remained unchanged. Diabetic NMRI developed the most pronounced hyperfiltration as well as increased oxidative stress and proteinuria but without glomerular damage. Diabetic BALB/c did not develop hyperfiltration but presented with pronounced proteinuria, increased oxidative stress, and glomerular damage. Diabetic 129Sv displayed proteinuria and increased oxidative stress without glomerular hyperfiltration or damage. However, all strains displayed intrastrain correlation between oxidative stress and proteinuria. In conclusion, diabetic C57Bl/6 and NMRI both developed glomerular hyperfiltration but neither presented with histological damage, although NMRI developed low-degree proteinuria. Thus these strains may be suitable when investigating the mechanism causing hyperfiltration. Neither BALB/c nor 129Sv developed hyperfiltration although both developed pronounced proteinuria. However, only BALB/c developed detectable histological damage. Thus BALB/c may be suitable when studying the roles of proteinuria and histological alterations for the progression of diabetic nephropathy.

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“…LPO derivatives and this weaken the antioxidant machinery system (SOD, CAT, and GPx) [ 37 , 38 ] in the kidney of DN rats. Kidney cells are more vulnerable to ROS mediated oxidative damage because of a high rate of oxygen consumptions [ 39 ]. Previously, we have reported that the STZ induced DN rats had clinical characteristics of increase proteinuria, urea and creatinine along with decreased creatinine clearance showed successful induction of DN and PTY-2r treatment significantly ameliorates these changes in a dose-dependent manner [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Antioxidant and Antiapoptotic effect of aqueous extract of Pueraria tuberosa (Roxb. Ex Willd.) DC. On streptozotocin-induced diabetic nephropathy in rats

Shukla

Banerjee

Tripathi

2018

BMC Complement Altern Med

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BackgroundOxidative stress and renal apoptosis play a significant role in the progression of diabetic nephropathy. The tubers of Pueraria tuberosa (Roxb. ex Willd.) DC. has been traditionally used as anti-ageing and health promotive tonic. The purpose of this study was to investigate its nephroprotective effect and mechanism via antioxidant and antiapoptotic potential in Streptozotocin-induced diabetic nephropathy (DN) in rats.MethodsThe chemical composition of aqueous extract of Pueraria tuberosa (PTY-2r) was analyzed by gas chromatography-mass spectrometry (GC-MS). Diabetes was induced by intraperitoneal injection of streptozotocin (STZ) (55 mg/kg body weight) in rats. After 60 days, the rats were randomly divided into 3 groups (n = 6/each group), namely DN control (DN) group-2, DN rats treated with PTY-2r at the dose of 50 mg/100 g, group-3 and 100 mg/100 g, group-4 p.o. for 20 days. The normal rats were chosen as a normal control (NC) group-1. PTY-2r was orally given to the rats for 20 days. Reactive oxygen species (ROS), lipid peroxidation (LPO) and the activity of ROS-scavenging enzymes – superoxide dismutase (SOD), catalase (CAT) & glutathione peroxidase (GPx) were determined in the kidney tissue of DN rats. The expression of apoptosis-related proteins was measured by immunofluorescence.ResultsGC-MS analysis of PTY-2r indicated the presence of 37 compounds among them 5-Hydroxymethylfurfural (17.80%), 2,3-dihydro-3,5-dihydroxy-6-methyl-4H-pyran-4-one (17.03%), n-Hexadecanoic acid (5.18%) and 9-Octadecenoic acid (Z) - (6.69%) were found in the higher amount. A significant increase in ROS and LPO was observed along with the decreased activity of antioxidant enzymes, responsible for oxidative stress in the kidney of DN rats. Since, high oxidative stress induces apoptosis in target cells, as shown by significantly decreased expression of Bcl-2 along with increased expression of Bax, active Caspase-3 & cleaved PARP-1 in DN control rats, suggesting apoptosis. The PTY-2r treatment significantly raised the activity of antioxidant enzymes, suppressed oxidative stress and apoptosis thus, prevented urinary albumin excretion in a dose-dependent manner.ConclusionsThe findings suggest that PTY-2r exerted the nephroprotective potential against STZ induced DN rats via suppressing oxidative stress and apoptosis due to the presence of different bioactive compounds.Graphical AbstractᅟElectronic supplementary materialThe online version of this article (10.1186/s12906-018-2221-x) contains supplementary material, which is available to authorized users.

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Oxidative Stress and Hypoxia in the Pathogenesis of Diabetic Nephropathy

Cited by 9 publications

References 224 publications

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes

Antioxidant and Antiapoptotic effect of aqueous extract of Pueraria tuberosa (Roxb. Ex Willd.) DC. On streptozotocin-induced diabetic nephropathy in rats

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