Key result
Neohesperidin significantly inhibited Angiotensin II-induced myocardial contractile dysfunction, cardiac hypertrophy, myocardial fibrosis, oxidative stress, and inflammation in mice and NRCMs.
Why the study?
The mechanism and role of Neohesperidin in cardiac hypertrophy and remodeling caused by Angiotensin II had not been fully elucidated.
Does neohesperidin prevent cardiac hypertrophy and remodeling in Angiotensin II-induced models?
Population
Mice with Ang II-induced cardiac hypertrophy and remodeling, and Ang II-induced NRCMs
Comparison
Neohesperidin treatment vs controls
Design
In vivo mouse and in vitro preclinical study
Authors
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Neohesperidin attenuates Ang II-induced remodeling in mice; leaves open any role in human cardiac hypertrophy pending clinical data.
Does neohesperidin prevent cardiac hypertrophy and remodeling in Angiotensin II-induced models?
Neohesperidin demonstrates potential as a therapeutic agent for preventing cardiac hypertrophy and remodeling in preclinical models.
Zhang et al. (2020) studied Cardiac hypertrophy and remodeling. Neohesperidin vs. Angiotensin II alone was evaluated on Myocardial contractile dysfunction, cardiac hypertrophy, myocardial fibrosis, myocardial oxidative stress and inflammation. Neohesperidin significantly inhibited Angiotensin II-induced myocardial contractile dysfunction, cardiac hypertrophy, myocardial fibrosis, oxidative stress, and inflammation in mice and NRCMs.
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