Rosiglitazona e lesão vascular em coelhos hipercolesterolêmicos: avaliação da formação neointimal

Alessi, Alexandre; Neto, Olímpio Ribeiro França; Prim, Camila; Silva, Ruy Fernando Kuenzer Caetano da; Noronha, Lúcia de; Brofman, Paulo Roberto Slud; Baroncini, Liz Andréa Villela; Précoma, Dalton Bertolim

doi:10.1590/s0066-782x2010005000101

Cited by 3 publications

(4 citation statements)

References 32 publications

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“…Previous reports have pointed out that PPAR-γ receptor agonists could prevent restenosis and atherosclerosis [14,24]. Similarly, in a recent study, PPAR-γ receptor ligand rosiglitazone was shown to decrease neointima and increase luminal area of the vessels after balloon catheter injury in collesterol-fed rabbits [25]. Besides, it was reported that rosiglitazone reduced inflammatory response and retarded neointima progression after vascular injury in experimental atherosclerosis models in mouse and rats [26].…”

Section: Discussionmentioning

confidence: 96%

The effects of PPARγ agonist rosiglitazone on neointimal hyperplasia in rabbit carotid anastomosis model

Guzeloglu

Reel

Atmaca

et al. 2012

J Cardiothorac Surg

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BackgroundNeointimal hyperplasia involving smooth muscle cell (SMC) proliferation, migration and extracellular matrix (ECM) degradation is an important component of atherosclerosis. It develops as a response to vascular injury after balloon angioplasty and vascular graft placement. Matrix metalloproteinases (MMPs) induce SMC proliferation, migration and contribute to intimal hyperplasia by degrading ECM. PPARγ agonists inhibit SMC proliferation, migration and lesion formation. In this study, we aimed to investigate the effects of PPARγ agonist rosiglitazone on neointimal hyperplasia and gelatinase (MMP-2 and MMP-9) expressions in rabbit carotid anastomosis model.MethodsNew Zealand white rabbits (n = 13, 2.7–3.2 kg) were divided into placebo and treatment groups. Right carotid artery (CA) was transected and both ends were anastomosed. Treatment group (n = 6) received rosiglitazone (3 mg/kg/day/p.o.) and placebo group (n = 7) received PBS (phosphate buffered saline, 2.5 ml/kg/day/p.o.) for 4 weeks postoperatively. After the sacrification, right and left CAs were isolated. Morphometric analyses and immunohistochemical examinations for gelatinases were performed.ResultsIntimal area (0.055 ± 0.005 control vs 0.291 ± 0.020 μm2 anastomosed, p < 0,05) and index (0.117 ± 0.002 control vs 0.574 ± 0.013 anastomosed, p < 0,01) significantly increased in anastomosed arteries compared to control arteries from placebo group. However, in rosiglitazone-treated group, intimal area (0.291 ± 0.020 PBS vs 0.143 ± 0.027 rosiglitazone, p < 0,05) and index (0.574 ± 0.013 PBS vs 0.263 ± 0.0078 rosiglitazone, p < 0,01) significantly decreased. Furthermore, gelatinase immunopositivity was found to have significantly increased in anastomosed arteries from placebo group and decreased with rosiglitazone treatment.ConclusionsThese results suggest that rosiglitazone may prevent neointimal hyperplasia, which is the most important factor involved in late graft failure, by inhibiting gelatinase enzyme expression.

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Section: Discussionmentioning

confidence: 96%

The effects of PPARγ agonist rosiglitazone on neointimal hyperplasia in rabbit carotid anastomosis model

Guzeloglu

Reel

Atmaca

et al. 2012

J Cardiothorac Surg

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“…That study is part of our research line in an animal model (rabbits) submitted to a hypercholesterolemic diet and then treated with functional food (linseed and resveratrol) 1 . Within our research line we also work with medications and arterial lesions in hypercholesterolemic rabbits 2,3 . All such models used rabbits, whose hypercholesterolemia had been caused by either the Sigma Aldrich product or lyophilized eggs.…”

Section: Response Lettermentioning

confidence: 99%

“…Studies with dietary formulations require the description of all components included in the diet, because they vary considerably in commercial formulations (especially antioxidants) and might jeopardize the results and reproducibility of the study 2 .…”

Section: Dear Editormentioning

confidence: 99%

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Resveratrol provoca efeitos antiaterogênicos em um modelo animal de aterosclerose

Novaes¹,

Pelúzio²,

Maldonado³

2012

Arq. Bras. Cardiol.

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Keywords:Atherosclerosis; models; animal; antioxidants; dyslipidemias. Dear Editor,We read with great interest the article by Matos et al. 1 and would like to comment on its protocol and results.Studies with dietary formulations require the description of all components included in the diet, because they vary considerably in commercial formulations (especially antioxidants) and might jeopardize the results and reproducibility of the study 2 .The absence of a group of animals treated with a standard diet with no lipid supplementation hinders the assessment of the predisposition of the animal model to develop atherosclerosis. That is a fundamental aspect considering the differential susceptibility to atherosclerosis of the strain of rabbits used 3 .The control animals had significantly increased baseline levels of total cholesterol and triglycerides as compared with those of the resveratrol-treated group (58% and 72%, respectively). Combining such results with the lack of statistical significance of the biochemical parameters at the end of the experiment, it seems unlikely that resveratrol can inhibit the formation of atherosclerotic lesions without changing the serum lipid parameters of the animals treated. In addition, the morphometric analysis performed does not represent a good indicator of the evolution of atherosclerotic processes, because the number and total area of the lesions are more reliable parameters 4 . Thus, we suggest that the results are difficult to interpret based on the limitations regarding the characterization of the animal model used, nutritional characteristics of the diet and methodology selected to assess atherosclerotic lesions. Response letter,We would like to thank the interest in our article and the pertinent questions raised. We shared those same doubts. That study is part of our research line in an animal model (rabbits) submitted to a hypercholesterolemic diet and then treated with functional food (linseed and resveratrol) 1 . Within our research line we also work with medications and arterial lesions in hypercholesterolemic rabbits 2,3 . All such models used rabbits, whose hypercholesterolemia had been caused by either the Sigma Aldrich product or lyophilized eggs. In other studies, we had a control group receiving only a normal diet for the species with no cholesterol added, but that group was not included in the present study.

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Rosiglitazone alleviates injury in rats with adenine-induced chronic kidney disease

Huang

Yan

Zheng

et al. 2013

Molecular Medicine Reports

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Abstract. Rosiglitazone (ROG) has been shown to exert beneficial effects on glycemic control and renal protection. Circulatory fibroblast growth factor-23 (FGF-23) is a novel independent risk factor for chronic kidney disease (CKD) progression. The current study focused on how ROG impacts on injury of the kidney, and whether FGF-23 is involved in the process. A total of 24 male Sprague Dawley rats, weighing 250-280 g, were divided into four groups (n=6 per group): i) Normal; ii) ROG controls, treated with ROG (10 mg/kg/day); iii) CKD models, treated with adenine (200 mg/kg/day); and iv) ROG treatment, treated with ROG (10 mg/kg/day) and adenine (200 mg/kg/day). The rats were sacrificed after four weeks, and serum, urine and kidney tissues were collected. The data revealed that the serum levels of inorganic phosphate (Pi), intact parathyroid hormone (iPTH) and FGF-23 were significantly higher in the CKD models compared with those in the normal group (P<0.01), while ROG significantly reduced the serum levels of Pi, iPTH and FGF-23 (P<0.01). The ratio of protein/creatine (Cr) in the urine and the serum levels of Cr, blood urea nitrogen and uric acid were significantly increased in the CKD models compared with the normal group (P<0.01), however, ROG significantly reduced these parameters (P<0.05). Furthermore, ROG significantly alleviated the tubule interstitial damage index of the CKD models in comparison with that of the controls. These results indicated that ROG mitigates the lesions of chronic kidney disease induced by adenine, and that the system of Pi-PTH-FGF-23 may contribute to this process. The possible mechanisms underlying this process require confirmation in future studies.

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Rosiglitazona e lesão vascular em coelhos hipercolesterolêmicos: avaliação da formação neointimal

Abstract: Background: Rosiglitazone has been the focus of extensive discussion.

Cited by 3 publications

References 32 publications

The effects of PPARγ agonist rosiglitazone on neointimal hyperplasia in rabbit carotid anastomosis model

The effects of PPARγ agonist rosiglitazone on neointimal hyperplasia in rabbit carotid anastomosis model

Resveratrol provoca efeitos antiaterogênicos em um modelo animal de aterosclerose

Rosiglitazone alleviates injury in rats with adenine-induced chronic kidney disease

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