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Updated: May 7, 2026
Transverse Aortic Constriction in Mice
Published on: April 21, 2010
Oltipraz ameliorates pressure overload-induced pathological cardiac hypertrophy in mice
Junmou Hong1, Huang Cao1, Yan Wang2
1Vascular Department of Xiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Abstract:
Oltipraz (OPZ), a synthetic dithiothiol, is regarded as a novel agonist of nuclear factor erythroid-2 (Nrf-2). Recent studies revealed that Nrf-2 activation could suppress the pathological cardiac hypertrophy in mice. However, the therapeutic role of OPZ in the pathological cardiac hypertrophy remains incompletely understood. Thus, we evaluated the cardioprotective effects of OPZ in vivo and in vitro. Transverse aortic constriction (TAC) surgery was performed to induce the pathological cardiac hypertrophy in mice. In addition, the H9c2 cells were treated with angiotensin II (Ang II) to induce cardiomyocyte hypertrophy in vitro experiments. Our data revealed that OPZ relieved the TAC-induced pathological cardiac hypertrophy and myocardial damage in mice. Similarly, OPZ mitigated the increase in cardiomyocyte size induced by Ang II, indicating its ability to counteract cardiomyocyte hypertrophy. In addition, OPZ reduces cardiomyocyte oxidative stress, inflammation and apoptosis by activating Nrf-2 signaling in vivo and in vitro. Interestingly, our results also demonstrated that Nrf-2 knockdown abolished the protective effects of OPZ in vitro. Taken together, these data revealed that OPZ ameliorates the pathological cardiac hypertrophy via activating Nrf-2 signaling.
Insights
Oltipraz (OPZ) protects against pathological cardiac hypertrophy by activating the Nrf-2 pathway. This compound reduces heart damage, inflammation, and cell death in both mouse models and cell cultures.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Pharmacology
Background:
- Pathological cardiac hypertrophy is a significant risk factor for heart failure.
- Nuclear factor erythroid-2 (Nrf-2) activation has shown potential in suppressing cardiac hypertrophy.
- The therapeutic efficacy of Oltipraz (OPZ) in cardiac hypertrophy requires further elucidation.
Purpose of the Study:
- To investigate the cardioprotective effects of Oltipraz (OPZ) in pathological cardiac hypertrophy.
- To determine the role of Nrf-2 signaling in OPZ-mediated cardioprotection.
Main Methods:
- Induction of cardiac hypertrophy in mice via transverse aortic constriction (TAC) surgery.
- Induction of cardiomyocyte hypertrophy in H9c2 cells using angiotensin II (Ang II).
- Assessment of OPZ effects on cardiac function, cell size, oxidative stress, inflammation, and apoptosis, with and without Nrf-2 knockdown.
Main Results:
- OPZ treatment attenuated TAC-induced cardiac hypertrophy and myocardial damage in mice.
- OPZ mitigated Ang II-induced cardiomyocyte hypertrophy in vitro.
- OPZ reduced cardiomyocyte oxidative stress, inflammation, and apoptosis by activating Nrf-2 signaling.
- Nrf-2 knockdown abrogated the protective effects of OPZ.
Conclusions:
- Oltipraz (OPZ) demonstrates significant cardioprotective effects against pathological cardiac hypertrophy.
- OPZ ameliorates cardiac hypertrophy by activating the Nrf-2 signaling pathway.
- These findings highlight OPZ as a potential therapeutic agent for cardiac hypertrophy.
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