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 | |
【 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.
【 授权许可】
CC BY
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