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Updated: Aug 15, 2026

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Published on: March 31, 2022

Andrographolide Mitigates DOCA-Salt-Induced Cardiac Hypertrophy by Regulating Calcium-Handling Genes

Muhamad Rizqy Fadhillah1,2,3, Wawaimuli Arozal2, Raymond Rubianto Tjandrawinata4

  • 1Doctoral Program in Biomedical Science, Universitas Indonesia, Central Jakarta, Java, Indonesia.

Journal of Pharmacy & Bioallied Sciences
|August 14, 2026
PubMed

Insights

Andrographolide treatment reduced cardiac hypertrophy in a rat model of hypertension. This natural compound helped restore normal calcium handling and reduce key markers of heart disease.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Molecular Biology

Background:

  • Cardiac hypertrophy is a detrimental response to chronic hypertension, often linked to calcium handling dysregulation.
  • Andrographolide, a plant-derived compound, shows promise for heart protection, but its effect on pressure-overload hypertrophy is not well understood.
  • This study investigates andrographolide's impact on hypertension-induced cardiac hypertrophy and associated molecular changes.

Purpose of the Study:

  • To evaluate the efficacy of andrographolide in mitigating cardiac hypertrophy induced by deoxycorticosterone acetate (DOCA)-salt treatment in rats.
  • To assess andrographolide's influence on calcium-handling gene expression, specifically SERCA2a and RyR.
  • To determine the effect of andrographolide on plasma B-type natriuretic peptide (BNP) levels as a biomarker for cardiac strain.

Main Methods:

  • A deoxycorticosterone acetate (DOCA)-salt rat model was established to induce hypertension and cardiac hypertrophy.
  • Rats were treated with andrographolide or a vehicle control after developing hypertension.
  • Cardiac function, blood pressure, plasma BNP, cardiac calcium levels, and SERCA2a/RyR mRNA expression were assessed.

Main Results:

  • DOCA-salt treatment led to significant increases in blood pressure, left ventricular hypertrophy, plasma BNP, and cardiac calcium levels.
  • Andrographolide administration effectively attenuated these hypertension-induced detrimental effects.
  • Andrographolide treatment restored the expression of SERCA2a and RyR, key calcium-handling proteins.

Conclusions:

  • Andrographolide demonstrates a significant therapeutic effect against DOCA-salt-induced cardiac hypertrophy in rats.
  • The cardioprotective mechanism of andrographolide appears to involve the restoration of calcium-handling pathways.
  • These findings suggest andrographolide holds potential for treating hypertension-related cardiac remodeling.
Abstract

Keywords:
Andrographolidecalcium handlingcardiac remodelinghypertension

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