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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-9827
Vol. 15, No. 11, 2016, pp. 2421-2427
Bioline Code: pr16319
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 15, No. 11, 2016, pp. 2421-2427

 en Role of hypoxia-inducible factor in diabetic myocardial hypertrophy
Qin, L; Xifa, S; Dawei, X; Yangjing, X; Kangting, J; Jian, X & Suqin, Z


Purpose: This study was carried out to investigate the role of hypoxia-inducible factor (HIF) in diabetic cardiomyopathy in vitro.
Methods: Hypoxia was induced chemically in H9C2 cells (cardiac hypertrophy model), and the cells were treated with phenylephrine (PE), deferoxamine (DFO), PE + DFO, and HIF-1α siRNA under conditions of high and normal glucose. Western blot was used to analyze the expression of some glycolytic proteins, including Glut-1, hexokinase (HXK-2), and enolase, while apoptosis of H9C2 was determined by flow cytometry.
Results: PE caused hypertrophy in H9C2, which was ameliorated by HIF-1α. Compared to normal, under prolonged high glucose, the low expression of HIF-1α led to low expressions of Glut-1, HXK-2 and enolase. However, expression of HIF-1α decreased, while those of Bax and Caspase 3 increased, and Bcl-2 expression decreased. Furthermore, under short time high glucose, HIF-1α caused apoptosis of hypertrophic cardiomyocytes.
Conclusion: HIF-1 mediates diabetic myocardial hypertrophy, probably as a function of the degree of high glucose exposure and hypoxia.

H9C2 cardiomyocyte; Hypoxia-inducible factor; Myocardial hypertrophy; Diabetic cardiomyopathy

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