Key result
Wedelolactone attenuates angiotensin II-induced cardiomyocyte hypertrophy and oxidative stress via Nrf2/HO-1 signaling.
Why the study?
The role and mechanism of Wedelolactone in myocardial hypertrophy are still unclear, and more effective drugs are needed to combat cardiomyocyte hypertrophy.
Wedelolactone demonstrates potential as an anti-hypertrophic agent by attenuating Angiotensin II-induced hypertrophy, oxidative stress, and apoptosis in cardiomyocytes via the Nrf2/HO-1 pathway in vitro.
Answers are grounded in this paper and cite their sources.
May support preclinical testing in hypertrophy models; leaves open any clinical role pending in vivo and human data.
Cardiomyocyte hypertrophy is the adaptive response of the heart to various physiological or pathological stresses. To combat this type of disease, more effective drugs are still needed. Wedelolactone is the main ingredient extracted from the medicinal plant Daylily and have effects such as immunomodulatory, anti-fibrosis, and anti-inflammation. However, the role and mechanism of Wedelolactone in myocardial hypertrophy are still unclear. Here, H9C2 cells were treated with Ang II to construct a cardiomyocyte hypertrophy cell model. We found Wedelolactone suppressed the survival of Ang II-induced cardiomyocytes. Wedelolactone further restrained the progression of Ang II-induced cardiomyocyte hypertrophy. Wedelolactone suppressed the oxidative stress of Ang II-induced cardiomyocytes, and restrained the apoptosis. Mechanically, Wedelolactone restrained the progression of Ang II-induced cardiomyocyte hypertrophy via Nuclear factor erythroid 2-related factor 2/Heme oxygenase-1 pathway (Nrf2/HO-1 pathway). In summary, Wedelolactone attenuates angiotensin II-induced hypertrophy and apoptosis in cardiomyocytes. Wedelolactone attenuates angiotensin II-stimulated hypertrophy and apoptosis in cardiomyocytes.
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Zhang et al. (2024) studied Cardiomyocyte hypertrophy. Wedelolactone vs. Angiotensin II alone was evaluated on Cardiomyocyte hypertrophy, oxidative stress, and apoptosis (p=<0.001). Wedelolactone attenuated angiotensin II-stimulated hypertrophy, oxidative stress, and apoptosis in H9C2 cardiomyocytes, mediated by the Nrf2/HO-1 pathway.
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