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Nelumbo nucifera Receptaculum Extract Suppresses Angiotensin II-Induced Cardiomyocyte Hypertrophy

 Soyoung Cho  ;  Hyun Woo Cho  ;  Kyeong Wan Woo  ;  Jisu Jeong  ;  Juyeon Lim  ;  Sungha Park  ;  Miran Seo  ;  Soyeon Lim 
 MOLECULES, Vol.24(9) : E1647, 2019 
Journal Title
Issue Date
Angiotensin II/metabolism* ; Angiotensin II/pharmacology ; Animals ; Biomarkers ; Cell Line ; Cell Survival/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hypertrophy ; Myocytes, Cardiac/drug effects* ; Myocytes, Cardiac/metabolism* ; Myocytes, Cardiac/pathology ; Nelumbo/chemistry* ; Oxidative Stress/drug effects ; Plant Extracts/chemistry ; Plant Extracts/pharmacology* ; Protein Kinase C/metabolism ; Rats ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects
Nelumbo nucifera receptaculum ; angiotensin II ; cardiomyocyte hypertrophy
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-H2DCFDA, a general oxidative stress indicator. Ang II-induced cardiomyocyte hypertrophy was significantly attenuated by 5 µg/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-κB 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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5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
Yonsei Authors
Park, Sung Ha(박성하) ORCID logo https://orcid.org/0000-0001-5362-478X
Seo, Mi Ran(서미란)
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