期刊论文详细信息
Frontiers in Cardiovascular Medicine
Traditional Chinese Medication Qiliqiangxin Attenuates Diabetic Cardiomyopathy via Activating PPARγ
article
Xiaodong Wu1  Ting Zhang1  Ping Lyu1  Mengli Chen1  Gehui Ni1  Huiling Cheng1  Guie Xu2  Xinli Li1  Lijun Wang2  Hongcai Shang3 
[1] Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University;Cardiac Regeneration and Ageing Lab, Shanghai Engineering Research Center of Organ Repair, School of Life Science, Institute of Cardiovascular Sciences, Shanghai University;Key Laboratory of Chinese Internal Medicine of Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese Medicine
关键词: Qiliqiangxin;    diabetic cardiomyopathy;    apoptosis;    fibrosis;    PPARγ;    PGC-1α;   
DOI  :  10.3389/fcvm.2021.698056
学科分类:地球科学(综合)
来源: Frontiers
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【 摘 要 】

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.

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