title: Attenuating effects of dihydromyricetin on angiotensin II-induced rat cardiomyocyte hypertrophy related to antioxidative activity in a NO-dependent manner.
abstract: BACKGROUND
  Dihydromyricetin (DMY) displays a range of biological properties. However, whether DMY attenuates cardiomyocyte hypertrophy is unknown.
  
  
  OBJECTIVE
  To investigate whether DMY had potential therapeutic value to protect against angiotensin II (Ang II)-induced cardiomyocyte hypertrophy.
  
  
  METHODS
  Neonatal rat cardiomyocytes were pretreated with DMY (0-320 μM) followed with Ang II (100 nM) stimulation for 24 h, and then degree of hypertrophy was evaluated by cell surface analysis. Levels of reactive oxygen species (ROS) were measured with 2',7'-dichlorfluorescein-diacetate (DCFH-DA) fluorescent staining. Antioxidative activity was evaluated by malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, and total antioxidant capacity (T-AOC). Cyclic guanosine monophosphate (cGMP) was determined with a radioimmunoassay.
  
  
  RESULTS
  Pre-incubation with DMY (20, 40, 80, and 160 μM) for 8 h, 12 h, 24 h, or 48 h decreased cell surface areas. It down-regulated mRNA expression of atrial natriuretic factor (1.95- to 1.24-fold) and β-myosin heavy chains (3.51- to 2.32-fold), reduced levels of MDA as well as increased SOD activity and T-AOC. Expression of SOD and thioredoxin were enhanced by DMY, whereas p22(phox) and phosphorylation of mitogen-activated protein kinases were inhibited. Content of cGMP (0.54- to 0.80-fold) and phosphorylation of endothelial nitric oxide synthase at serine 1177 (0.70- to 1.05-fold) were augmented by DMY. Moreover, attenuating effect of DMY on hypertrophy was abolished when NO production was inhibited by l-NAME.
  
  
  CONCLUSIONS
  Attenuating effects of DMY on Ang II-induced cardiomyocyte hypertrophy related to antioxidative activity in a NO-dependent manner.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Nantong University , Nantong, Jiangsu , China and.
authors.forename: Guoliang
authors.initials: G
authors.lastname: Meng
authors.forename: Shengju
authors.initials: S
authors.lastname: Yang
authors.forename: Yun
authors.initials: Y
authors.lastname: Chen
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Yao
authors.forename: Hongyan
authors.initials: H
authors.lastname: Zhu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000494:pharmacology; D048429:Cell Size / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D006152:Cyclic GMP / Q000378:metabolism; D044948:Flavonols / Q000494:pharmacology*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects*; D009569:Nitric Oxide / Q000737:chemistry*; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000378:metabolism; D061251:Primary Cell Culture; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D044948:Flavonols; D017382:Reactive Oxygen Species; D000804:Angiotensin II; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D020928:Mitogen-Activated Protein Kinases; D006152:Cyclic GMP; C472036:dihydromyricetin
keywords: Cyclic guanosine monophosphate; endothelial nitric oxide synthase; mitogen-activated protein kinase; reactive oxygen species