Ganoderma lucidum polysaccharides attenuates pressure-overload-induced pathological cardiac hypertrophy

Changlin Zhen1,2, Xunxun Wu3, Jing Zhang1,2

  • 1Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area, Chongqing, China.

Insights

Ganoderma lucidum polysaccharides (GLPs) effectively treat pathological cardiac hypertrophy by inhibiting key genes involved in hypertrophy and fibrosis. This natural compound activates the PPARγ pathway, offering potential for heart failure treatment.

Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Natural Products Research

Background:

  • Pathological cardiac hypertrophy is a significant risk factor for cardiovascular disease.
  • Current drug therapies for reversing cardiac hypertrophy and restoring heart function are limited.
  • Ganoderma lucidum polysaccharides (GLPs) are bioactive compounds from Ganoderma lucidum with diverse pharmacological effects.

Purpose of the Study:

  • To investigate the therapeutic potential of GLPs in ameliorating cardiac hypertrophy.
  • To elucidate the molecular mechanisms underlying the cardioprotective effects of GLPs.

Main Methods:

  • Cardiac hypertrophy was induced in mice via transverse aortic constriction (TAC).
  • Cardiomyocyte hypertrophy was induced by Angiotensin II (Ang II) in vitro.
  • Gene expression analysis focused on hypertrophic and fibrotic markers, including the PPARγ/PGC-1α pathway.

Main Results:

  • GLPs demonstrated efficacy in ameliorating Ang II-induced cardiomyocyte hypertrophy in vitro.
  • GLPs significantly attenuated pressure overload-induced cardiac hypertrophy in vivo.
  • GLPs downregulated mRNA levels of hypertrophic and fibrotic markers, indicating inhibition via the PPARγ/PGC-1α pathway.

Conclusions:

  • GLPs inhibit pathological cardiac hypertrophy by downregulating key genes associated with hypertrophy and fibrosis.
  • Activation of the PPARγ pathway by GLPs plays a crucial role in attenuating pressure overload-induced cardiac hypertrophy.
  • These findings support the potential use of GLPs as a therapeutic agent for pathological myocardial hypertrophy and heart failure.

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