Open AccessBlueberry anthocyanin‑enriched extract ameliorates transverse aortic constriction‑induced myocardial dysfunction via the DDAH1/ADMA/NO signaling pathway in mice
Author(s) -
Weiqing Hu,
Wenyue Wang,
Qing Ma,
Tao Liu,
Jiefeng Zhang,
Jicun Zhang
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10800
Subject(s) - oncogene , molecular medicine , anthocyanin , cell cycle , apoptosis , constriction , signal transduction , signaling proteins , cardiology , cancer research , microbiology and biotechnology , medicine , biology , chemistry , biochemistry , botany
Blueberry anthocyanin‑enriched extract (BAE) has been demonstrated to protect against cardiovascular diseases by activating multiple target genes. The present study investigated the effects of BAE on transverse aortic constriction (TAC)‑induced myocardial dysfunction in mice and explored its possible molecular mechanisms. A total of 30 male mice were divided randomly into control, TAC and TAC + BAE groups. Mice in the TAC + BAE groups were administered BAE by oral gavage for 6 consecutive weeks. Myocardial dysfunction was assessed using echocardiogram, histopathology, TUNEL assay, immunofluorescence staining, reverse transcription‑quantitative PCR and western blot analysis. The results demonstrated that BAE treatment significantly ameliorated heart weight, left ventricular weight, myocardial dysfunction, left ventricular hypertrophy and fibrosis. In addition, BAE treatment alleviated TAC‑induced inflammation, oxidative stress and apoptosis. Notably, BAE treatment markedly reduced asymmetric dimethylarginine (ADMA) concentration and significantly increased dimethylarginine dimethylaminohydrolase 1 (DDAH1) expression and nitric oxide (NO) production. The present data indicated that BAE treatment ameliorated TAC‑induced myocardial dysfunction, oxidative stress, inflammatory response and apoptosis via the DDAH1/ADMA/NO signaling pathway.