Article Publish Status: FREE
Abstract Title:

Galangin ameliorates cardiac remodeling via the MEK1/2-ERK1/2 and PI3K-AKT pathways.

Abstract Source:

J Cell Physiol. 2019 Feb 11. Epub 2019 Feb 11. PMID: 30741414

Abstract Author(s):

Hui-Bo Wang, Si-Hui Huang, Man Xu, Jun Yang, Jian Yang, Ming-Xin Liu, Chun-Xia Wan, Hai-Han Liao, Di Fan, Qi-Zhu Tang

Article Affiliation:

Hui-Bo Wang


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.

Study Type : Animal Study

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