PLoS ONE (Jan 2014)

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

  • Chih-Hsien Wang,
  • Ru-Wen Chang,
  • Ya-Hui Ko,
  • Pi-Ru Tsai,
  • Shoei-Shen Wang,
  • Yih-Sharng Chen,
  • Wen-Je Ko,
  • Chun-Yi Chang,
  • Tai-Horng Young,
  • Kuo-Chu Chang

DOI
https://doi.org/10.1371/journal.pone.0090471
Journal volume & issue
Vol. 9, no. 3
p. e90471

Abstract

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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.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.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.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.