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Updated: May 12, 2026

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
Published on: September 25, 2017
20(S)-protopanaxatriol ameliorates cardiac hypertrophy by activating the AMPK/PGC-1α/PPARγ signaling pathway
Xue Yan1, Huajie Zheng1, Ju Ye1
1State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, The MOE Key Laboratory of Standardization of Chinese Medicines, The SATCM Key Laboratory of New Resources and Quality Evaluation of Chinese Medicines, The Shanghai Key Laboratory for Compound Chinese Medicines, Institute of Chinese Materia Medica and Shanghai Frontiers Science Center of TCM Chemical Biology, Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Background:
Pathological cardiac hypertrophy, a critical precursor to heart failure, presents a significant therapeutic challenge. The triterpenoid 20(S)-protopanaxatriol (PPT), derived from Panax ginseng Meyer, exhibits antioxidant, anti-inflammatory, and neuroprotective properties. However, its efficacy against cardiac hypertrophy and the underlying molecular mechanisms remain unclear, limiting clinical translation.
Methods:
We evaluated PPT's anti-hypertrophic effects in murine models of transverse aortic constriction (TAC), phenylephrine (PE)-infusion, and myocardial infarction (MI). In vitro analyses assessed oxidative stress and mitochondrial function in neonatal rat cardiomyocytes (NRCMs). Network pharmacology identified targets, with AMPK inhibitors validating pathway involvement.
Results:
Among 18 tested ginsenosides, PPT demonstrated the strongest anti-hypertrophic activity in vitro. In murine models, PPT attenuated myocardial remodeling, improved echocardiographic parameters, and delayed heart failure progression. Mechanistically, PPT suppressed ROS, enhanced mitochondrial biogenesis, and promoted fatty acid oxidation through AMPK/PGC-1α/PPARγ activation.
Conclusion:
PPT mitigates cardiac hypertrophy by modulating oxidative stress, mitochondrial function, and energy metabolism through AMPK/PGC-1α/PPARγ signaling, highlighting its therapeutic promise for cardiac pathologies.
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