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

PLoS One. 2014 Mar 4;9(3):e90471. doi: 10.1371/journal.pone.0090471. eCollection 2014.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arginine / analogs & derivatives
  • Arginine / metabolism
  • Atorvastatin
  • Blood Glucose / metabolism
  • Blood Pressure / drug effects
  • Body Weight / drug effects
  • C-Reactive Protein / metabolism
  • Cholesterol / blood
  • Diabetes Mellitus, Experimental / blood
  • Diabetes Mellitus, Experimental / metabolism*
  • Diabetes Mellitus, Experimental / physiopathology*
  • Dose-Response Relationship, Drug
  • Fatty Acids / blood
  • Glycation End Products, Advanced / metabolism
  • Hemodynamics / drug effects
  • Heptanoic Acids / administration & dosage*
  • Heptanoic Acids / pharmacology*
  • Lysine / analogs & derivatives
  • Lysine / metabolism
  • Male
  • Malondialdehyde / blood
  • Malondialdehyde / metabolism*
  • Organ Size / drug effects
  • Pyrroles / administration & dosage*
  • Pyrroles / pharmacology*
  • Rats, Wistar
  • Streptozocin
  • Vascular Stiffness / drug effects*

Substances

  • Blood Glucose
  • Fatty Acids
  • Glycation End Products, Advanced
  • Heptanoic Acids
  • Pyrroles
  • Malondialdehyde
  • Streptozocin
  • C-Reactive Protein
  • Arginine
  • Cholesterol
  • Atorvastatin
  • pentosidine
  • Lysine

Grants and funding

This study was supported by grants from the National Science Council of Taiwan (NSC 101-2320-B-002-021-MY2) and National Taiwan University Hospital, Hsin-Chu Branch (HCH-101-19). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.