Background:
Diabetic cardiomyopathy is the primary complication associated with
diabetes mellitus and also is a major cause of death and disability. Limited pharmacological
therapies are available for
diabetic cardiomyopathy.
Qiliqiangxin (QLQX), a Chinese medication, has been proven to be beneficial for
heart failure patients. However, the role and the underlying protective mechanisms of QLQX in
diabetic cardiomyopathy remain largely unexplored. Methods: Primary neonatal rat cardiomyocytes (NRCMs) were treated with
glucose (HG, 40 mM) to establish the
hyperglycemia-induced apoptosis model in vitro.
Streptozotocin (STZ, 50 mg/kg/day for 5 consecutive days) was intraperitoneally injected into mice to establish the
diabetic cardiomyopathy model in vivo. Various analyses including qRT-PCR, western blot, immunofluorescence [
terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining] histology (
hematoxylin-
eosin and Masson's trichrome staining), and cardiac function (echocardiography) were performed in these mice. QLQX (0.5 μg/ml in vitro and 0.5 g/kg/day in vivo) was used in this study. Results: QLQX attenuated
hyperglycemia-induced cardiomyocyte apoptosis via activating peroxisome proliferation-activated receptor γ (PPARγ). In vivo, QLQX treatment protected mice against STZ-induced cardiac dysfunction and pathological remodeling. Conclusions: QLQX attenuates
diabetic cardiomyopathy via activating PPARγ.