Journal
CLINICAL AND EXPERIMENTAL HYPERTENSION
Volume 39, Issue 7, Pages 672-679Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/10641963.2017.1313853
Keywords
Akt; AMPK; angiogenesis; berberine; miR-29b; myocardial infarction
Funding
- National Natural Science Foundation of China [81470591, 81570723, 81673423]
- Natural Science Foundation of Henan Province [162300410216, 121100910300, 132102310247]
- Research Fund of Xinxiang Medical University [2016PN-KFKT-02, XYBSKYZZ201626, 2014QN153, ZD2011-30]
- Taihang Young Scholars of Xinxiang Medical University
Ask authors/readers for more resources
Background: Berberine has several preventive effects on cardiovascular diseases. Increased expression of miR-29b has been reported to attenuate cardiac remodeling after myocardial infarction (MI). We hypothesized that berberine via an miR-29b-dependent mechanism promotes angiogenesis and improves heart functions in mice after MI. Methods: The MI model was established in mice by ligation of left anterior descending coronary artery. The expression of miR-29b was examined by RT-qPCR. Angiogenesis was assessed by immunohistochemistry. Results: Berberine increased miR-29b expression and promoted cell proliferations and migrations in cultured endothelial cells, which were abolished by miR-29b antagomir or AMP-activated protein kinase inhibitor compound C. In mice following MI, administration of berberine significantly increased miR-29b expressional level, promoted angiogenesis, reduced infarct size, and improved heart functions after 14 postoperative days. Importantly, these in vivo effects of berberine were ablated by antagonism of miR-29b. Conclusion: Berberine via upregulation of miR-29b promotes ischemia-induced angiogenesis and improves heart functions.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available