Premium
Galangin ameliorates cardiac remodeling via the MEK1/2–ERK1/2 and PI3K–AKT pathways
Author(s) -
Wang HuiBo,
Huang SiHui,
Xu Man,
Yang Jun,
Yang Jian,
Liu MingXin,
Wan ChunXia,
Liao HaiHan,
Fan Di,
Tang QiZhu
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28216
Subject(s) - galangin , protein kinase b , pi3k/akt/mtor pathway , pressure overload , fibrosis , inflammation , medicine , ventricular remodeling , cardiac fibrosis , kinase , pharmacology , muscle hypertrophy , endocrinology , signal transduction , chemistry , biology , microbiology and biotechnology , myocardial infarction , biochemistry , cardiac hypertrophy , quercetin , kaempferol , antioxidant
Cardiac remodeling is associated with inflammation and apoptosis. Galangin, as a natural flavonol, has the potent function of regulating inflammation and apoptosis, which are factors related to cardiac remodeling. Beginning 3 days after aortic banding (AB) or Sham surgery, mice were treated with galangin for 4 weeks. Cardiac remodeling was assessed according to echocardiographic parameters, histological analyses, and hypertrophy and fibrosis markers. Our results showed that galangin administration attenuated cardiac hypertrophy, dysfunction, and fibrosis response in AB mice and angiotensin II‐treated H9c2 cells. The inhibitory action of galangin in cardiac remodeling was mediated by MEK1/2–extracellular‐regulated protein kinases 1/2 (ERK1/2)–GATA4 and phosphoinositide 3‐kinase (PI3K)–protein kinase B (AKT)–glycogen synthase kinase 3β (GSK3β) activation. Furthermore, we found that galangin inhibited inflammatory response and apoptosis. Our findings suggest that galangin protects against cardiac remodeling through decreasing inflammatory responses and apoptosis, which are associated with inhibition of the MEK1/2–ERK1/2–GATA4 and PI3K–AKT–GSK3β signals.