Elsevier

Life Sciences

Volume 64, Issue 12, 12 February 1999, Pages 1029-1036
Life Sciences

Lack of regression of atherosclerotic lesions in phytosterol-treated apo E-deficient mice

https://doi.org/10.1016/S0024-3205(99)00029-6Get rights and content

Abstract

We evaluated the effects of a phytosterol mixture (FCP-3PI) on the regression of atherosclerotic lesions in male apo E-deficient mice. Atherosclerosis was induced in fifteen mice by a “Western-type” diet containing 9% (w/w) fat and 0.15% (w/w) cholesterol over a period of 18 weeks (Induction phase). Then, two mice were used to evaluate the development of atherosclerosis, and the rest was divided into the control (n = 6) and treated (n = 7) groups. The control group was fed mouse chow (4.5% w/w fat) and the treated group fed the same chow supplemented with 2% (w/w) FCP-3PI for an additional 25 weeks (Regression phase). The mice developed severe hypercholesterolemia and advanced atherosclerotic lesions over the induction phase. During the first 6 weeks of regression phase, plasma cholesterol concentrations decreased at a similar rate (35%) in both groups of control and phytosterol-treated mice. Although evidence of lesion regression was not observed in either group of mice, the treated group had slightly smaller lesion size than the controls. During the induction phase, each mouse developed atherosclerotic lesions averaging 0.025 mm2 per week. However, during the regression phase, this was decreased to approximately one fifth and one third in the treated and control groups, respectively. Thus, compared to the end of the induction phase, the control group had a 40% increase in the lesion size, while this increase was only 28% in the treated animals. In conclusion, our previous findings along with a small decrease in the atherosclerotic lesion size observed in the treated group in the present study suggest that FCP-3PI treatment may slow the development of atherosclerotic lesions in apo E-deficient mice; however, a longer regression period may yield a greater benefit.

References (24)

  • R.J. Nicolosi et al.

    Atherosclerosis

    (1998)
  • W.V. Rodrigueza et al.

    Biochim. Biophys. Acta

    (1998)
  • W. Hollander et al.

    Exp. Mol. Pathol.

    (1979)
  • D. Vesselinovitch et al.

    Atherosclerosis.

    (1974)
  • T.B. Clarkson et al.

    Exp. Mol. Pathol.

    (1981)
  • T.B. Clarkson et al.

    Exp. Mol. Pathol.

    (1984)
  • M.H. Criqui et al.

    Am. J. Epidemiol.

    (1989)
  • T. Kita et al.

    Am. J. Cardiol.

    (1988)
  • A.M. Gotto

    Circulation

    (1995)
  • J.W. Jukema et al.

    Circulation

    (1995)
  • Y. Nakashima et al.

    Arterioscler. Thromb.

    (1994)
  • S.H. Zhang et al.

    Science

    (1992)
  • Cited by (52)

    • Plant-derived bioactives

      2019, Comprehensive Biotechnology
    • Postprandial plasma oxyphytosterol concentrations after consumption of plant sterol or stanol enriched mixed meals in healthy subjects

      2015, Steroids
      Citation Excerpt :

      The controversy around the potential atherogenicity of plant sterols might relate to the question whether plant sterols are oxidized or not. We and others have previously shown that in transgenic mouse models plant sterol enriched diets lower atherosclerotic lesion development [7–9] while enrichment with oxidized plant sterols (oxyphytosterols) resulted in larger and more severe atherosclerotic lesions [10]. Data regarding origin, metabolism, pathophysiological effects and effects of specific diets on oxyphytosterol metabolism in humans are however scarce.

    • Dietary phytosterol does not accumulate in the arterial wall and prevents atherosclerosis of LDLr-KO mice

      2013, Atherosclerosis
      Citation Excerpt :

      One study found that homozygous ABCG5/G8-KO mice without PS supplementation had higher plasma PS concentrations; this increase was not related to the development of atherosclerotic lesion areas [11]. Other studies conducted with apoE-KO mice fed a PS-enriched diet showed that PS plasma concentrations are positively or negatively [12,13] related to the development of atherosclerosis and may inhibit the regression of existing lesions [14]. In agreement with the results of the latter study, an investigation conducted in heterozygous LDLr-KO mice fed PS with or without atorvastatin failed to show an atherogenic effect [15].

    • Plant Derived Bioactives

      2011, Comprehensive Biotechnology, Second Edition
    • Phytosterols and atherosclerosis

      2011, Revue de Medecine Interne
    View all citing articles on Scopus
    View full text