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August 6, 2026Pharmacological Research - Modern Chinese MedicineOpen Access

Andrographolide attenuates salt-sensitive cardiac hypertrophy and restores mitochondrial alterations in a rat model.

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Why the study?

Although andrographolide has cardioprotective properties, its effects on mitochondrial quality control during hypertensive cardiac remodelling remain unclear.

Does andrographolide mitigate salt-sensitive cardiac remodeling in a UNX-DOCA-salt rat model?

Population

Male Sprague-Dawley rats subjected to the UNX-DOCA-salt model

Comparison

Andrographolide vs spironolactone

Design

Animal experimental study with computational validation

Key result

Andrographolide at 30 mg/kg body weight attenuated salt-sensitive cardiac hypertrophy and restored structural and mitochondrial alterations in a UNX-DOCA-salt rat model.

Authors

MFMuhamad Rizqy FadhillahVJValdi Ven JapranataRTRaymond R. Tjandrawinata

Discussion

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Overview

May support MQC modulation in preclinical hypertrophy models; hypothesis-generating, clinical translation remains untested.

Key Points

  • To investigate whether andrographolide attenuates salt-sensitive cardiac hypertrophy by modulating mitochondrial quality control and apoptosis-associated signaling pathways.
  • Male Sprague-Dawley rats subjected to the uninephrectomy-deoxycorticosterone acetate-salt (UNX-DOCA-salt) model received andrographolide (30 or 60 mg/kg) or spironolactone.
  • Cardiac hypertrophy and mitochondrial function were assessed via organ weights, cardiomyocyte cross-sectional area, succinate dehydrogenase activity, calcium levels, and RT-qPCR.
  • Partial least squares regression, correlation analysis, molecular docking, and MM/GB(PB)SA simulations computationally evaluated drug-target interactions.
  • UNX-DOCA-salt induced marked cardiac hypertrophy, mitochondrial dysfunction, and significant upregulation of DRP1, PINK1, PGC-1α, TFAM, p53, and BNP.
  • Andrographolide at 30 mg/kg body weight restored structural, mitochondrial, and transcriptional parameters more consistently than the 60 mg/kg dose.
  • Computational modeling identified DRP1 as the primary driver of remodeling and confirmed energetically favorable binding of andrographolide within the DRP1 GTPase-binding domain.

Structured PICO

Does andrographolide mitigate salt-sensitive cardiac remodeling in a UNX-DOCA-salt rat model?

P
Population
Male Sprague-Dawley rats subjected to the UNX-DOCA-salt model of cardiac hypertrophy.
I
Intervention
Andrographolide (30 mg/kg or 60 mg/kg body weight)
C
Comparator
Spironolactone or untreated UNX-DOCA-salt model
O
Outcome
Cardiac hypertrophy assessed by cardiac weight, cardiac weight-to-body weight ratio, and cardiomyocyte cross-sectional areasurrogate

Andrographolide attenuates salt-sensitive cardiac hypertrophy in rats, likely through modulation of mitochondrial homeostasis and DRP1-mediated dynamics.

Cite This Study

Fadhillah et al. (2026) studied salt-sensitive cardiac hypertrophy. Andrographolide vs. spironolactone was evaluated on Cardiac hypertrophy and mitochondrial function. Andrographolide at 30 mg/kg body weight attenuated salt-sensitive cardiac hypertrophy and restored structural and mitochondrial alterations in a UNX-DOCA-salt rat model.

synapsesocial.com/papers/6a83729ecaa63b238dc94c9ahttps://doi.org/10.1016/j.prmcm.2026.100855
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