Nelumbo nucifera Receptaculum Extract Suppresses Angiotensin II-Induced Cardiomyocyte Hypertrophy

被引:9
|
作者
Cho, Soyoung [1 ]
Cho, Hyun Woo [2 ]
Woo, Kyeong Wan [2 ]
Jeong, Jisu [1 ]
Lim, Juyeon [1 ]
Park, Sungha [3 ]
Seo, Miran [4 ]
Lim, Soyeon [5 ]
机构
[1] Yonsei Univ, Grad Program Sci Aging, Seoul 120752, South Korea
[2] Natl Dev Inst Korean Med, Korean Med Herbs Res Team, 288 Udeuraendeu Gil, Jangheung Gun 59337, Jeollanam Do, South Korea
[3] Yonsei Univ, Coll Med, Div Cardiol, Cardiovasc Res Inst, Seoul 120752, South Korea
[4] Yonsei Univ, Coll Med, Severance Integrat Res Inst Cerebral & Cardiovasc, Seoul 120752, South Korea
[5] Catholic Kwandong Univ, Coll Med, Inst Biomed Convergence, Kangnung 25601, Gangwon Do, South Korea
来源
MOLECULES | 2019年 / 24卷 / 09期
基金
新加坡国家研究基金会;
关键词
Nelumbo nucifera receptaculum; angiotensin II; cardiomyocyte hypertrophy; LEFT-VENTRICULAR HYPERTROPHY; INDUCED CARDIAC-HYPERTROPHY; FACTOR-KAPPA-B; NADPH OXIDASE; BETA-SITOSTEROL; ACTIVATION;
D O I
10.3390/molecules24091647
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nelumbo nucifera Gaertn. (lotus) is an important medicinal plant, and many parts of the plant have been investigated for their therapeutic effects. However, the therapeutic effect of receptacles of lotuses on pathological cardiomyocyte hypertrophy has not been investigated yet. Therefore, the current study aimed to determine the protective effect of lotus against angiotensin II (Ang II)-induced cardiomyocyte hypertrophy in vitro. Ang II was used to induce hypertrophy of H9c2 cells. The lotus receptacle powder (MeOH extract of receptaculum Nelumbinis; MRN) used in the experiments was prepared by MeOH extraction and subsequent evaporation. To evaluate the effect of MRN on cardiomyocyte hypertrophy, cell size, protein synthesis, and hypertrophic marker expressions were examined. The antioxidant ability of MRN was determined by using CM-H(2)DCFDA, a general oxidative stress indicator. Ang II-induced cardiomyocyte hypertrophy was significantly attenuated by 5 mu g/mL of MRN, as confirmed by the reductions in cell size, protein synthesis, and hypertrophic marker expression. MRN also attenuated Ang II-induced excessive intracellular reactive oxygen species (ROS) production through the suppression of protein kinase C (PKC), extracellular-signal-regulated kinase (ERK), and NF-B activation and subsequent type I angiotensin receptor (AT1R), receptor for advanced glycation end products (RAGE), and NADPH oxidase (NOX) expression. MRN exerted a significant protective effect against Ang II-induced cardiomyocyte hypertrophy through suppression of PKC-ERK signaling, and this subsequently led to attenuation of intracellular ROS production.
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页数:11
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