Traditional Chinese Medication Qiliqiangxin Attenuates Diabetic Cardiomyopathy via Activating PPARγ.
Traditional Chinese Medication Qiliqiangxin Attenuates Diabetic Cardiomyopathy via Activating PPARγ.
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中药芪苈强心通过激活 PPARγ 减轻糖尿病心肌病
DOI：
10.3389/fcvm.2021.698056
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发表时间：
2021
影响因子：
3.6
通讯作者：
Shang H
中科院分区：
文献类型：
--
作者：
Wu X;Zhang T;Lyu P;Chen M;Ni G;Cheng H;Xu G;Li X;Wang L;Shang H
背景：糖尿病心肌病是糖尿病相关的主要并发症，也是死亡和残疾的主要原因。可用于糖尿病心肌病的药物疗法有限。芪苈强心（QLQX）是一种中药，已被证明对心力衰竭患者有益。然而，QLQX 在糖尿病心肌病中的作用和潜在的保护机制在很大程度上仍未被探索。方法：用葡萄糖（HG，40 mM）处理原代新生大鼠心肌细胞（NRCM），建立高血糖诱导的体外凋亡模型。将链脲佐菌素（STZ，50 mg/kg/天，连续5 d）腹腔注射给小鼠，建立体内糖尿病心肌病模型。对这些小鼠进行了各种分析，包括 qRT-PCR、蛋白质印迹、免疫荧光[末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记 (TUNEL) 染色]组织学（苏木精-伊红和马森三色染色）和心脏功能（超声心动图）。本研究中使用了 QLQX（体外 0.5 μg/ml，体内 0.5 g/kg/天）。结果：QLQX 通过激活过氧化物酶体增殖激活受体 γ (PPARγ) 减弱高血糖诱导的心肌细胞凋亡。在体内，QLQX 治疗可保护小鼠免受 STZ 诱导的心脏功能障碍和病理重塑。结论：QLQX 通过激活 PPARγ 减轻糖尿病心肌病。
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.