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An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
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17-β Oestradiol prevents cardiovascular dysfunction in post-menopausal metabolic syndrome by affecting SIRT1/AMPK/H3

Dhaval Sharad Bendale1, Pinakin Arun Karpe, Richa Chhabra

  • 1Laboratory of Chromatin Biology, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Mohali, Punjab, India.

British Journal of Pharmacology
|July 6, 2013
PubMed
Abstract

Insights

17-β estradiol (E2) therapy mitigates cardiovascular dysfunction in post-menopausal metabolic syndrome (PMS) by restoring SIRT1/AMPK signaling and reducing cardiac apoptosis. This suggests E2 may prevent cardiovascular disorders in PMS.

Area of Science:

  • Endocrinology
  • Cardiovascular Physiology
  • Epigenetics

Background:

  • Post-menopausal metabolic syndrome (PMS) is linked to increased cardiovascular risk.
  • Oestrogen therapy is known to offer cardioprotection in PMS.

Purpose of the Study:

  • To investigate the effects of 17-β oestradiol (E2) on angiotensin II responses and cardiovascular dysfunction in a rat model of PMS.
  • To elucidate the underlying molecular mechanisms involving SIRT1/AMPK and epigenetic modifications.

Main Methods:

  • Post-menopausal metabolic syndrome (PMS) was induced in ovariectomized rats via a high-fat diet.
  • Isometric tension of aortic rings and endothelial function were assessed.
  • Apoptosis and protein expression (AT1 receptors, Bax, PARP, SIRT1, P-AMPK, H3 acetylation) were analyzed using TUNEL assay and immunoblotting.

Main Results:

  • PMS rats exhibited endothelial dysfunction, increased AT1 receptor expression, cardiac apoptosis, and altered SIRT1/AMPK/H3 acetylation.
  • E2 treatment partially reversed angiotensin II-induced contractions, normalized SIRT1/P-AMPK levels, and reduced H3 acetylation.
  • Inhibition of SIRT1/AMPK exacerbated angiotensin II responses and abolished E2's protective effects.

Conclusions:

  • Cardiovascular dysfunction in PMS involves SIRT1/AMPK and histone H3 acetylation pathways.
  • E2 exerts cardioprotective effects by modulating these pathways.
  • Targeting SIRT1/AMPK and epigenetic modifications may offer therapeutic strategies for cardiovascular disease prevention in PMS.
Keywords:
AMPKSIRT1post-menopausal metabolic syndrome

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