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Effects of quercetin on mitochondrial function and dynamics in process of improving myocardial cell hypertrophy
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DOI   10.11656/j.issn.1672-1519.2019.01.22
Key Words   quercetin;cardiocyte;hypertrophy;mitochondria
Author NameAffiliationE-mail
WU Shun Department of Endocrinology, People's Hospital of Xinzhou District, Wuhan 430400, China  
CHEN Mingjun Department of Endocrinology, People's Hospital of Xinzhou District, Wuhan 430400, China  
ZHOU Yan Department of Cardiology, People's Hospital of Xinzhou District, Wuhan 430400, China 57896136@qq.com 
Abstract
    [Objective] To observe the effects of quercetin on the cell hypertrophy, mitochondrial function and dynamics in cardiocytes.[Methods] Primary myocardial cells were cultured with angiotensin Ⅱ (Ang Ⅱ) and quercetin for 48 or 72 h. The total protein content was detected using BCA kit, and cell diameter was measured by inverted microscope. The contents of adenosine triphosphate (ATP) and reactive oxygen species (ROS) in cardiocytes were detected using microplate reader. Mitochondrial membrane potential (MMP) was measured by JC-1. Mitochondrial optic atrophy (OPA1), dynamin-related protein 1 (DRP1) and phosphorylation dynamin-related 1 (p-Drp1) was determined by Western Blot assay.[Results] Compared with control group, the total protein content, cell diameter and ROS were greatly increased in model group, while the ATP and MMP were significantly decreased (P<0.05). Western Blot results indicated that the expression of OPA1 significantly decreased, while the expression of p-Drp1 greatly increased in model group (P<0.05). Compared with model group, the total protein content, cell diameter and ROS were greatly decreased in cardiocytes after treatment with quercetin for 72 h, while the ATP and MMP were significantly increased (P<0.05). Western Blot results indicated that the expression of OPA1 significantly increased, while the expression of p-Drp1 greatly decreased in in cardiocytes after treatment with quercetin for 72 h (P<0.05).[Conclusion] Quercetin can improve myocardial cell hypertrophy induced by Ang Ⅱ, and the mechanism may related to alleviating myocardial mitochondrial dysfunction and dynamic unbalance.

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