Effect of Cerivastatin on Endothelial Dysfunction and Aortic CD36 Expression in Diabetic Hyperlipidemic Rats

Nakamura, Toshio; Saito, Yuichiro; Ohyama, Yoshio; Uchiyama, Tsuyoshi; Sumino, Hiroyuki; Kurabayashi, Masahiko

doi:10.1291/hypres.27.589

Cited by 7 publications

(3 citation statements)

References 32 publications

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“…For example the treatment with pravastatin didn’t show effects on the uptake of modified lipoproteins by macrophages derived from hipercholesterolemic subjects [27]. It is noteworthy also that in rats with metabolic disorders the cerivastatin therapy led to increased expression of CD36 receptors [32]. Oppositely, the findings obtained from in vitro studies on the effects of fluvastatin, simvastatin or lovastatin therapy on the level of scavenger receptors expression demonstrated that the drugs significantly decreased the expression of LOX-1, SRA-I, SRA-II and CD36 [13, 24, 35, 40, 41].…”

Section: Discussionmentioning

confidence: 99%

Highly Upregulated Expression of CD36 and MSR1 in Circulating Monocytes of Patients with Acute Coronary Syndromes

Piechota

Banaszewska

Dudziak³

et al. 2012

Protein J

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Acute Coronary Syndromes (ACS) are a group of disorders caused by the significant reduction of circulation in coronary arteries. The most common reason of the dysfunction is a blood clot formed in place of plaque rupture. The role of scavenger receptors in development and progression of atherosclerosis has been confirmed in many animal experiments, however the knowledge about contribution of the receptors in the development of ACS symptoms in humans still remains insufficient. The aim of this work was to define the expression of two scavenger receptors: CD36 and MSR1 in monocytes of patients with ACS after the onset of symptoms and after the 6 months of treatment. The analysis of CD36 and MSR1 expression was carried out with the use of real-time PCR and flow cytometry. Analyses of lipid and glucose concentration in blood and the level of inflammatory markers in plasma were performed additionally for all ACS patients. All data obtained during the research were analyzed using statistical tests, such as Mann Whitney test, Wilcoxon test, or correlation. In all patients with symptoms of ACS the amount of CD36 and MSR1 mRNA in circulating monocytes, as well as the density of both receptors on the cells surface was significantly higher. Re-analysis of subjects after 6 months of treatment, showed a significant decrease in the CD36 and MSR1 expression in all patients who received atorvastatin. The results of presented studies demonstrate that both investigated receptors are involved in the development and/or progression of ACS.

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Section: Discussionmentioning

confidence: 99%

Highly Upregulated Expression of CD36 and MSR1 in Circulating Monocytes of Patients with Acute Coronary Syndromes

Piechota

Banaszewska

Dudziak³

et al. 2012

Protein J

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“…Also, pravastatin was shown to decrease BP in spontaneously hypertensive rats (SHR) (9). The antihypertensive effect of HMG-CoA reductase inhibitors may be due to an improvement in endothelial function (30). Indeed, a higher dose of statin was shown to promote endothelial NO synthase protein expression (31).…”

Section: Discussionmentioning

confidence: 99%

Renoprotective Effect of Pravastation in Salt-Loaded Dahl Salt-Sensitive Rats

et al. 2005

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The pathophysiological features of nephrosclerosis may be analogous to those of atherosclerosis, which is intimately related to lipid metabolism. Thus, we examined whether a lipid-lowering agent, pravastatin, would ameliorate renal damage in hypertensive model animals. Salt-loaded Dahl salt-sensitive (S) rats were given pravastatin (2 mg/ml in drinking water) for 5 weeks. Pravastatin decreased systolic blood pressure. Although pravastatin did not influence the serum total, high-density, or low-density lipoprotein cholesterol, serum triglycerides were decreased. Pravastatin decreased urinary protein excretion and ameliorated histopathological damage in salt-loaded Dahl S rats. Increased urinary excretion of 8-iso-prostagaldin F2S and 8-hydroxy-2 ′ -deoxyguanosine and renal superoxide overproduction and decreased reduced glutathione in the renal parenchyma were ameliorated with pravastatin in Dahl S rats fed a high salt diet. Therefore, pravastatin

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“…Of these, a new dihydropyridine CCB, azelnidipine, has a unique, highly lipophilic chemical structure and appears to slowly enter a lipid compartment surrounding the dihydropyridine binding site; and it has a long-lasting vasodilatory effect (5). In the present study, we assessed the effects of azelnidipine on the expression of the mineralocorticoid receptor (MCR), angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor (AT 1 R) genes in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a useful model of obese type II diabetes characterized by hypertension, hypertriglyceridemia, hyperinsulinemia, hyperglycemia, insulin resistance, and abundant visceral fat (6,7).…”

mentioning

confidence: 99%

Azelnidipine Down-Regulates Renal Angiotensin-Converting Enzyme and Mineralocorticoid Receptor mRNA in Diabetic Hypertensive Rats

Nakamura¹,

Saito²,

Saito³

et al. 2006

J Pharmacol Sci

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Abstract. Effects of a new lipophilic L-type calcium channel blocker, azelnidipine, on the expression of molecular components of the renin-angiotensin-aldosterone system (RAAS) were assessed. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of diabetes with hypertension, and their lean littermates, Long-Evans Tokushima Otsuka (LETO) rats, were treated with azelnidipine for 2 weeks. The renal cortical mineralocorticoid receptor mRNA in OLETF was higher than in LETO, but was suppressed (P<0.05) by azelnidipine. Renal cortical angiotensin-converting enzyme mRNA of OLETF was lower than that of LETO rats, and it was further suppressed by azelnidipine (P<0.05). Azelnidipine can down-regulate the gene expression of molecular components of RAAS.

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Effect of Cerivastatin on Endothelial Dysfunction and Aortic CD36 Expression in Diabetic Hyperlipidemic Rats

Cited by 7 publications

References 32 publications

Highly Upregulated Expression of CD36 and MSR1 in Circulating Monocytes of Patients with Acute Coronary Syndromes

Highly Upregulated Expression of CD36 and MSR1 in Circulating Monocytes of Patients with Acute Coronary Syndromes

Renoprotective Effect of Pravastation in Salt-Loaded Dahl Salt-Sensitive Rats

Azelnidipine Down-Regulates Renal Angiotensin-Converting Enzyme and Mineralocorticoid Receptor mRNA in Diabetic Hypertensive Rats

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