The Prevention of Diabetic Cardiomyopathy by Non-Mitogenic Acidic Fibroblast Growth Factor Is Probably Mediated by the Suppression of Oxidative Stress and DamageReport as inadecuate




The Prevention of Diabetic Cardiomyopathy by Non-Mitogenic Acidic Fibroblast Growth Factor Is Probably Mediated by the Suppression of Oxidative Stress and Damage - Download this document for free, or read online. Document in PDF available to download.

Background

Emerging evidence showed the beneficial effect of acidic fibroblast growth factor aFGF on heart diseases. The present study investigated whether non-mitogenic aFGF nm-aFGF can prevent diabetic cardiomyopathy and the underlying mechanisms, if any.

Methodology-Principal Findings

Type 1 diabetes was induced in mice by multiple intraperitoneal injections of low-dose streptozotocin. Hyperglycemic and age-matched control mice were treated with or without nm-aFGF at 10 µg-kg daily for 1 and 6 months. Blood pressure and cardiac function were assessed. Cardiac H9c2 cell, human microvascular endothelial cells, and rat cardiomyocytes were exposed to high glucose 25 mM for mimicking an in vitro diabetic condition for mechanistic studies. Oxidative stress, DNA damage, cardiac hypertrophy and fibrosis were assessed by real-time qPCR, immunofluorescent staining, Western blotting, and pathological examination. Nm-aFGF significantly prevented diabetes-induced hypertension and cardiac dysfunction at 6 months. Mechanistic studies demonstrated that nm-aFGF showed the similar preventive effect as the native aFGF on high glucose-induced oxidative stress increase generation of reactive oxygen species and damage cellular DNA oxidation, cell hypertrophy, and fibrotic response increased mRNA expression of fibronectin in three kinds of cells. These in vitro findings were recaptured by examining the heart of the diabetic mice with and without nm-aFGF.

Conclusions

These results suggest that nm-aFGF can prevent diabetic cardiomyopathy, probably through attenuation of cardiac oxidative stress, hypertrophy, and fibrosis.



Author: Chi Zhang, Linbo Zhang, Shali Chen, Biao Feng, Xuemian Lu, Yang Bai, Guang Liang, Yi Tan, Minglong Shao, Melissa Skibba, Litai Ji

Source: http://plos.srce.hr/



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