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  4. Prevention of arterial stiffening by using low-dose atorvastatin in diabetes is associated with decreased malondialdehyde
 
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Prevention of arterial stiffening by using low-dose atorvastatin in diabetes is associated with decreased malondialdehyde

Journal
PLoS ONE
Journal Volume
9
Journal Issue
3
Date Issued
2014
Author(s)
CHIH-HSIEN WANG  
Chang R.-W.
Ko Y.-H.
Tsai P.-R.
SHOEI-SHEN WANG  
YIH-SHARNG CHEN  
Ko W.-J.
Chang C.-Y.
Tai-Horng Young  
KUO-CHU CHANG  
DOI
10.1371/journal.pone.0090471
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84897084613&doi=10.1371%2fjournal.pone.0090471&partnerID=40&md5=52d77063275e1125d308687f67614d9a
https://scholars.lib.ntu.edu.tw/handle/123456789/434010
Abstract
Introduction: Without affecting the lipid profile, a low-dose treatment with atorvastatin contributes to the reduction of oxidative stress, inflammation, and adverse cardiovascular events in diabetes. In this study, we investigated whether low-dose atorvastatin exerts any beneficial effect on vascular dynamics in streptozotocin (STZ)-induced diabetes in male Wistar rats. Methods: Diabetes was induced using a single tail-vein injection of STZ at 55 mg kg-1. The diabetic rats were treated daily with atorvastatin (10 mg kg-1 by oral gavage) for 6 weeks. They were also compared with untreated age-matched diabetic controls. Arterial wave reflection was derived using the impulse response function of the filtered aortic input impedance spectra. A thiobarbituric acid reactive substances measurement was used to estimate the malondialdehyde content. Results: The high plasma level of total cholesterol in the diabetic rats did not change in response to this low-dose treatment with atorvastatin. Atorvastatin resulted in a significant increase of 15.4% in wave transit time and a decrease of 33.5% in wave reflection factor, suggesting that atorvastatin may attenuate the diabetes-induced deterioration in systolic loads imposed on the heart. This was in parallel with its lowering of malondialdehyde content in plasma and aortic walls in diabetes. Atorvastatin therapy also prevented the diabetes-related cardiac hypertrophy, as evidenced by the diminished ratio of left ventricular weight to body weight. Conclusion: These findings indicate that low-dose atorvastatin might protect diabetic vasculature against diabetes-associated deterioration in aorta stiffness and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived malondialdehyde. ? 2014 Wang et al.
SDGs

[SDGs]SDG3

Other Subjects
atorvastatin; C reactive protein; cholesterol; fatty acid; malonaldehyde; thiobarbituric acid reactive substance; advanced glycation end product; arginine; atorvastatin; C reactive protein; cholesterol; fatty acid; glucose blood level; heptanoic acid derivative; lysine; malonaldehyde; pentosidine; pyrrole derivative; streptozocin; animal experiment; animal model; animal tissue; arterial stiffness; article; chemoprophylaxis; cholesterol blood level; controlled study; diabetes mellitus; diabetic angiopathy; dose response; down regulation; drug efficacy; drug mechanism; drug targeting; fatty acid blood level; heart hemodynamics; heart hypertrophy; impedance cardiography; lipid oxidation; low drug dose; male; nonhuman; rat; rat model; streptozotocin-induced diabetes mellitus; systolic blood pressure; analogs and derivatives; animal; arterial stiffness; blood; blood pressure; body weight; drug effects; experimental diabetes mellitus; glucose blood level; hemodynamics; metabolism; organ size; pathophysiology; Wistar rat; Animals; Arginine; Blood Glucose; Blood Pressure; Body Weight; C-Reactive Protein; Cholesterol; Diabetes Mellitus, Experimental; Dose-Response Relationship, Drug; Fatty Acids; Glycosylation End Products, Advanced; Hemodynamics; Heptanoic Acids; Lysine; Male; Malondialdehyde; Organ Size; Pyrroles; Rats, Wistar; Streptozocin; Vascular Stiffness
Publisher
Public Library of Science
Type
journal article

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