Animal Model of Adenine-Induced Chronic Renal Failure in Rats

Yokozawa, Takako; Zheng, Ping; Oura, Hikokíchi; Koizumi, Fumitomo

doi:10.1159/000183992

Cited by 310 publications

(268 citation statements)

References 9 publications

(10 reference statements)

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“…In the present study, adenine-fed rats exhibited severe renal failure with massive albuminuria and subsequent hypertension and hypercholesterolemia. A histopathological assessment of the kidneys showed progressive proximal tubular dilation and atrophic glomeruli (data not shown), similar to a previous report 14) . The renal failure rats showed extensive Human VSMCs were treated with or without high-dose (2.6 μM) inorganic phosphate (Pi) for six days.…”

Section: Inhibitory Effects Of the Statinsupporting

confidence: 90%

“…Renal failure was induced by feeding rats a 0.75% adenine-containing diet as described previously 14) . In brief, 12-week-old male Wistar rats (Nippon Clea Inc., Tokyo, Japan) were pair-fed standard CE-2 chow (containing 1.2% calcium and 0.6% phosphorus; Nippon Clea Inc.) in the control group or CE-2 chow containing 0.75% adenine (Sigma) in the renal failure group for six weeks.…”

Section: Experimental Renal Failure Ratsmentioning

confidence: 99%

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Pravastatin and Olmesartan Synergistically Ameliorate Renal Failure-Induced Vascular Calcification

Iijima

Ito

Son

et al. 2014

JAT

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Aim: Vascular calcification is a critical problem in patients with chronic kidney disease (CKD). In this study, we examined the effects of a HMG Co-A reductase inhibitor (statin) and an angiotensin Ⅱ type 1 receptor blocker (ARB) on renal failure-induced vascular calcification. Method and Result: Severe renal failure was induced in rats by feeding a 0.75% adenine diet for six weeks. These rats had hyperphosphatemia, hypertension and hypercholesterolemia. A histological assessment showed extensive linear calcification in the aortic media and a significant increase in the aortic content of calcium and phosphorus. Oral administration of pravastatin (a statin; 1-10 mg/kg/ day) or olmesartan (an ARB; 1-10 mg/kg/day) dose-dependently inhibited the aortic calcification in parallel with their renoprotective, lipid-lowering and blood pressure-lowering effects. Of note, the lowest dose of pravastatin inhibited aortic calcification with no influence on the renal function, BP and cholesterol, suggesting that it has direct vasoprotective properties. Intriguingly, the combined administration of pravastatin and olmesartan at the lowest doses synergistically ameliorated the aortic calcification, and the protective effect was at least partly attributable to the inhibition of RFinduced apoptosis in the aortic wall. An in vitro model of inorganic phosphate (Pi)-induced vascular smooth muscle cell calcification mimicked these effects of pravastatin and olmesartan, and the beneficial effect of the combination was attributable to the inhibitory effects on Pi-induced apoptosis via the restoration of the Gas6/Axl-mediated anti-apoptotic pathway. Conclusion: A statin and an ARB exerted potent protective effects against vascular calcification due to CKD, probably through their pleiotropic effects. In addition, combination therapy with pravastatin and olmesartan may provide a new therapeutic strategy for the prevention of vascular calcification.J Atheroscler Thromb, 2014; 21:917-929.

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Section: Inhibitory Effects Of the Statinsupporting

confidence: 90%

Section: Experimental Renal Failure Ratsmentioning

confidence: 99%

Pravastatin and Olmesartan Synergistically Ameliorate Renal Failure-Induced Vascular Calcification

Iijima

Ito

Son

et al. 2014

JAT

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“…The development of diabetes in these mice has several phases, with AGE levels being not elevated until the final stage characterised by hypoinsulinaemia and increasing hyperglycaemia [27]. The second model was that of chronic kidney failure induced by 4 weeks of treatment with adenine [28,29]. The subsequent uraemia is associated with high AGE levels without hyperglycaemia and within a metabolic milieu dissimilar to diabetes.…”

Section: Resultsmentioning

confidence: 99%

Advanced glycation end-products (AGEs) and functionality of reverse cholesterol transport in patients with type 2 diabetes and in mouse models

et al. 2012

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Aims/hypothesis We investigated the contribution of AGEs to the impairment of reverse cholesterol transport (RCT) variables in diabetic individuals and in two animal models of diabetic obesity and of renal impairment. Methods The capacity of plasma and HDL from 26 individuals with moderately controlled type 2 diabetes to support cholesterol efflux was compared with 26 age-and sexmatched individuals without diabetes. We also compared the rates of RCT in vivo in two animal models: db/db mice and mice with chronic renal failure. Results Diabetic individuals had characteristic dyslipidaemia and higher levels of plasma AGEs. The capacity of whole plasma, ApoB-depleted plasma and isolated HDL to support cholesterol efflux was greater for diabetic patients compared with controls despite their lower HDL-cholesterol levels. The capacity of plasma to support cholesterol efflux correlated with plasma levels of cholesteryl ester transfer protein and levels of ApoB, but not with levels of AGE. RCT was severely impaired in db/db mice despite elevated HDL-cholesterol levels and no change in AGE concentration, whereas RCT in uraemic mice was unaffected despite elevated AGE levels. Conclusions/interpretation AGEs are unlikely to contribute significantly to the impairment of RCT in type 2 diabetes.

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“…It was previously reported that adenine-treated kidneys were markedly enlarged with a pale gray color with the formation of foreign body granuloma in the tubular lamina and the interstitium of the kidney. 19 The model of adenine-induced CRF was developed by Yokozawa et al, 10 in which long-term feeding of adenine to rats produced metabolic abnormalities resembling CRF in humans. In mammalian metabolism, when it is present in excess, adenine becomes a significant substrate for xanthine dehydrogenase, which can oxidize adenine to 2,8-dihydroxyadenine (DHA).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Efficacy of Ginger, Arabic Gum, andBoswelliain Acute and Chronic Renal Failure

2011

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This study was conducted to evaluate the effects of Zingiber officinale Roscoe (Ginger), Arabic gum (AG), and Boswellia on both acute and chronic renal failure (CRF) and the mechanisms underlying their effects. Acute renal failure was induced by 30 min ischemia followed by 24 h reperfusion, while CRF was induced by adenine feeding for 8 weeks. Prophylactic oral administration of ginger, AG, Boswellia, or vehicle (in control groups) was started 3 days before and along with adenine feeding in different groups or 7 days before ischemia-reperfusion. Ginger and AG showed renoprotective effects in both models of renal failure. These protective effects may be attributed at least in part to their anti-inflammatory properties as evident by attenuating serum C-reactive protein levels and antioxidant effects as evident by attenuating lipid peroxidation marker, malondialdehyde levels, and increasing renal superoxide dismutase activity. Ginger was more potent than AG in both models of renal failure. However, Boswellia showed only partial protective effect against both acute renal failure and CRF and it had no antioxidant effects. Finally, we can say that ginger and AG could be beneficial adjuvant therapy in patients with acute renal failure and CRF to prevent disease progression and delay the need for renal replacement therapy.

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Animal Model of Adenine-Induced Chronic Renal Failure in Rats

Cited by 310 publications

References 9 publications

Pravastatin and Olmesartan Synergistically Ameliorate Renal Failure-Induced Vascular Calcification

Pravastatin and Olmesartan Synergistically Ameliorate Renal Failure-Induced Vascular Calcification

Advanced glycation end-products (AGEs) and functionality of reverse cholesterol transport in patients with type 2 diabetes and in mouse models

Evaluation of the Efficacy of Ginger, Arabic Gum, andBoswelliain Acute and Chronic Renal Failure

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