期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 41, 期 6, 页码 2503-2512出版社
KARGER
DOI: 10.1159/000475942
关键词
Diabetic cardiomyopathy; Empagliflozin; Endoplasmic reticulum stress
资金
- Science and Technology Program of Science and Technology Agency, Liaoning Province [2013225049]
- National Special Fund For Clinical Medicine Research [L2012057]
Background/Aims: This study aimed to determine whether or not the sodium-glucose cotransporter 2 inhibitor, empagliflozin (EMPA), can protect against diabetic cardiomyopathy (DCM) and to elucidate the related mechanism. Methods: Rats were divided into the following four groups: a non-diabetic group; diabetic cardiomyopathy rats without EMPA treatment; and diabetic cardiomyopathy rats with EMPA treatment (low-and high-dose EMPA). Hemodynamic measurements were performed to evaluate left ventricular systolic and diastolic function. The histopathology of the heart was examined with hematoxylin-eosin staining. Expression of glucose-regulated protein (GRP) 78, enhancer-binding protein homologous protein (CHOP), and caspase-12 was detected by Western blot, and the mRNA levels of XBP1, ATF4, and TRAF2 were analysed by real-time PCR. Results: EMPA significantly decreased the blood glucose level when compared with vehicle. EMPA strongly improved cardiac function based on hemodynamic and histopathologic analyses. Moreover, EMPA can significantly down-regulate the expression of GRP78, CHOP, and caspase-12 (P < 0.01). Additionally, the mRNA levels of XBP1, ATF4, and TRAF2 were markedly decreased by administration of EMPA (P < 0.01). Conclusion: EMPA protects against DCM by inactivating the endoplasmic reticulum stress pathway. (C) 2017 The Author(s) Published by S. Karger AG, Basel
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