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Flores-Castillo C.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | Zamora-Perez J.A.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | Carreon-Torres E.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | Carreon-Torres E.,Study Group of Atherosclerosis | And 12 more authors.
Fundamental and Clinical Pharmacology | Year: 2015

The anti-atherogenic properties of high-density lipoproteins (HDLs) may be related to their structure and metabolism. The HDL physicochemical characteristics that determine their plasma clearance during treatment with statins and fibrates are not well understood. In this study, we analyzed HDL-apo AI fractional catabolic rates (FCRs), size distributions, and the lipid composition of the HDL subclasses in New Zealand white rabbits with exogenous dyslipidemia that received low doses of atorvastatin and fenofibrate. Hypercholesterolemia decreased only partially with the combination of both drugs. HDL size distribution shifted toward larger particles among the groups of rabbits that received atorvastatin, fenofibrate, or their combination, compared with both the control group and the dyslipidemic group. The HDL subclasses were significantly rich in cholesterol in each of the groups compared with controls. The structural changes noted in the HDL subclasses were not associated with impaired plasma paraoxonase-1 (PON1) activity. The groups receiving monotherapy and the drug combination group were all associated with a higher apo AI FCR value compared with both the dyslipidemic rabbits and the control group. In conclusion, the combination of atorvastatin and fenofibrate induced a more favorable HDL subclass profile than did the individual use of these drugs. Similarly, the apo AI FCR values were augmented in every group receiving drug treatment (either monotherapy or combination therapy) in the setting of hypercholesterolemia. The anti-atherogenic properties of HDLs, excluding their capacity to bind PON1, may be enhanced by the structural and metabolic modifications induced by the combination of atorvastatin and fenofibrate. © 2015 Société Française de Pharmacologie et de Thérapeutique. Source


Perez-Torres I.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | El Hafidi M.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | Pavon N.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | Infante O.,Instituto Nacional Of Cardiologia Ignacio Chavez Juan Badiano 1 | And 2 more authors.
Metabolism: Clinical and Experimental | Year: 2010

Influence of sex on arachidonic acid metabolism, a pathway involved in the link between metabolic syndrome (MS) and renal damage, was studied in isolated perfused kidney. Metabolic syndrome was induced by feeding 30% sucrose solution for 24 weeks to intact and gonadectomized female (Ovx) and male (Cas) rats. Systolic blood pressure, albuminuria, as well as prostaglandin E2 and thromboxane B2 from urine and perfusate increased in MS male and MS ovariectomized females; castration reduced them in MS males. Perfusion of arachidonic acid in kidneys from MS males increased perfusion pressure compared with controls. No difference appeared in perfusion pressure between control and MS females. Castration diminished perfusion pressure in MS; the opposite was observed in Ovx MS. Perfusion with arachidonic acid plus indomethacin decreased perfusion pressure in MS male kidneys and in Cas MS. In Ovx MS, arachidonic acid plus indomethacin decreased perfusion pressure, but not in female control, MS, and Ovx control. Increase in perfusion pressure with arachidonic acid in both male MS and Ovx MS was related to cyclooxygenase (COX)-1 and COX-2 overexpression in kidney. Castration reduced the expression of COX-1 and COX-2 in MS to control levels. The results suggest that the alteration in arachidonic acid metabolism associated with changes in the expression of COX-1 and COX-2 induced by sucrose intake, and influenced by sex hormones, may contribute to renal damage. © 2010 Elsevier Inc. All rights reserved. Source

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