July 16, 2021Frontiers in Cardiovascular MedicineOpen Access

Traditional Chinese Medication Qiliqiangxin Attenuates Diabetic Cardiomyopathy via Activating PPARγ

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Why the study?

Limited pharmacological therapies exist for diabetic cardiomyopathy, and the role and protective mechanisms of Qiliqiangxin in diabetic cardiomyopathy remain largely unexplored.

Structured PICO

Population

Primary neonatal rat cardiomyocytes (NRCMs) exposed to high glucose (40 mM) and male mice with streptozotocin (STZ, 50 mg/kg/day for 5 days)-induced diabetic cardiomyopathy.

Intervention

Qiliqiangxin (QLQX) 0.5 μg/ml in vitro (48 h pretreatment) and 0.5 g/kg/day in vivo (intragastric administration for 8 weeks).

Comparator

Normal glucose (5.5 mM) in vitro; saline via intragastric administration in vivo.

Outcome

Cardiomyocyte apoptosis, cardiac dysfunction (echocardiography parameters including E/A ratio, EF, FS), and pathological remodeling.surrogate

Qiliqiangxin attenuates diabetic cardiomyopathy and hyperglycemia-induced cardiomyocyte apoptosis by activating PPARγ in preclinical models.

Limitations

QLQX contains 11 distinct active components, unclear which is the predominant cardioprotective factor or if there are cooperative effects
In vitro model used 48h pretreatment, unclear if shorter pretreatment or post-treatment would be effective

Implication

QLQX effects in rat cardiomyocytes remain hypothesis-generating; human trials needed before any clinical consideration.

Abstract

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.