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AdipoRon prevents l-thyroxine or isoproterenol-induced cardiac hypertrophy through regulating the AMPK-related

Xinlei Hu1, Qiong Ou-Yang1, Lanlan Wang1

  • 1Jiangsu Key Lab of Drug Screening and Jiangsu Key Lab of Metabolic Disease and Drug Discovery, China Pharmaceutical University, Nanjing, China.

Acta Biochimica Et Biophysica Sinica
|December 20, 2018
PubMed

Insights

AdipoRon treatment reversed cardiac hypertrophy in rats, reducing heart weight and BNP levels. This effect is partly mediated by activating the AMPK-related pathway, suggesting AdipoRon

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Cardiac hypertrophy is a significant risk factor for heart failure.
  • Understanding molecular pathways involved in cardiac hypertrophy is crucial for developing therapeutic strategies.
  • AdipoRon's potential role in mitigating cardiac hypertrophy requires investigation.

Purpose of the Study:

  • To investigate whether AdipoRon attenuates isoprenaline (ISO) or l-thyroxine-induced cardiac hypertrophy in Sprague-Dawley rats.
  • To determine if the anti-hypertrophy effect of AdipoRon is mediated by the AMPK-related pathway.

Main Methods:

  • Cardiac hypertrophy was induced in Sprague-Dawley rats using ISO or l-thyroxine.
  • AdipoRon was co-administered to the treatment group.
  • Measurements included heart and left ventricular weight, serum BNP levels, cardiac hypertrophy markers (ANP, BNP), and protein/mRNA expression of key signaling molecules (PGC-1α, ERRα, pAMPK/AMPK) via RT-PCR and Western blot.

Main Results:

  • AdipoRon significantly reversed the increase in heart weight/body weight ratio, left ventricular/body weight ratio, serum BNP, and ANP/BNP mRNA levels induced by ISO or l-thyroxine.
  • ISO or l-thyroxine reduced ERRα, PGC-1α mRNA/protein levels, and pAMPK/AMPK protein levels.
  • AdipoRon treatment restored the levels of pAMPK/AMPK, ERRα, and PGC-1α, indicating activation of the AMPK-related pathway.

Conclusions:

  • AdipoRon effectively attenuates cardiac hypertrophy induced by ISO or l-thyroxine in rats.
  • The anti-hypertrophic effects of AdipoRon are partly mediated through the activation of the AMPK-related pathway.
  • AdipoRon demonstrates potential as a therapeutic agent for preventing cardiac hypertrophy.

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