Dendrobium officinale Attenuates Myocardial Fibrosis via Inhibiting EMT Signaling Pathway in HFD/STZ-Induced Diabetic Mice

被引:33
作者
Zeng, Jie [1 ]
Li, Dongning [1 ]
Li, Zhubo [1 ]
Zhang, Jie [2 ]
Zhao, Xiaoyan [1 ]
机构
[1] Southwest Univ, Coll Pharmaceut Sci, Chongqing 400716, Peoples R China
[2] Chongqing Med Univ, Dept Neurol, Affiliated Hosp 2, Chongqing 400000, Peoples R China
关键词
Dendrobium officinale; diabetic cardiomyopathy; fibrosis; epithelial mesenchymal transition; MESENCHYMAL TRANSITION CONTRIBUTES; INSULIN-RESISTANCE; OXIDATIVE STRESS; CARDIOMYOPATHY; POLYSACCHARIDES; INFLAMMATION; ACTIVATION; MECHANISMS; EXPRESSION; KIMURA;
D O I
10.1248/bpb.b19-01073
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cardiac fibrosis is a major contributor for diabetic cardiomyopathy and Dendrobium officinale possessed therapeutic effects on hyperglycemia and diabetic cardiomyopathy. To further investigate the possible mechanisms of the Dendrobium officinale on diabetic myocardial fibrosis in mice. Water-soluble extracts of Dendrobium officinale (DOE) from dry stem was analyzed by HPLC and phenol-sulfuric acid method. Diabetic mice were induced by intraperitoneal injection of streptozotocin (STZ) (30mg/kg) for 4 consecutive days after intragastric administration of a high-fat diet (HFD) for 2 weeks. The groups were as follows: control group, model group, DOE low, medium, high dose group (75, 150, 300 mg/kg) and Metformin positive group (125mg/kg). The results showed that DOE dose-dependently lower serum insulin, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and grew the high-density lipoprotein cholesterol (HDL-C) after 12 weeks of daily administration with DOE. Hematoxylin-eosin staining and Sirius red staining showed obvious amelioration of cardiac injury and fibrosis. In addition, the result of immunoblot indicated that DOE increased the expression of peroxisome proliferator activated receptor-alpha (PPAR-alpha), phosphorylation of insulin receptor substrate 1 (p-IRS1) and E-cadherin and repressed the expression of transforming growth factor beta 1 (TGF-beta 1), phosphorylation of c-Jun N-terminal kinase (p-JNK), Twist, Snail1 and Vimentin. The present findings suggested that DOE ameliorated HFD/STZ-induced diabetic cardiomyopathy (DCM). The possible mechanism mainly associated with DOE accelerating lipid transport, inhibiting insulin resistant and suppressing fibrosis induced by epithelial mesenchymal transition (EMT).
引用
收藏
页码:864 / 872
页数:9
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