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吴华英,夏帅帅,黄惠勇,潘继兴,李静,贺佐梅,邵峰,曾光.加味生脉补心丹对2型糖尿病大鼠心肌损伤的保护作用[J].湖南中医药大学学报英文版,2019,39(4):453-458.[Click to copy
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| 加味生脉补心丹对2型糖尿病大鼠心肌损伤的保护作用 |
| 吴华英,夏帅帅,黄惠勇,潘继兴,李静,贺佐梅,邵峰,曾光 |
| (湖南中医药大学中医诊断学湖南省重点实验室, 湖南 长沙 410208;长沙市中医医院, 湖南 长沙 410005;湖南中医药大学中西医结合学院, 湖南 长沙 410208) |
| 摘要: |
| 目的 探讨加味生脉补心丹（以下简称BXD）对自发性非肥胖2型糖尿病Goto-kakisaki （GK）大鼠心肌损伤的保护作用。方法 8~9周龄雄性Wistar大鼠8只作为空白组，另将40只糖尿病模型GK大鼠按随机数字表将大鼠分为5组，分别为：模型组、西药组（格列齐特缓释片组）、BXD低剂量组、BXD中剂量组、BXD高剂量组。各组大鼠按治疗方法给药10周后处死，腹主动脉采血检测空腹血糖（FPG）、糖化血红蛋白（HbAlc）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA），取左心室行心肌组织HE染色、PAS染色观察病理改变，免疫组化测定心肌凋亡相关蛋白Bax、Bcl-2的表达。结果 与空白组比较，模型组FPG、HbAlc显著升高（P<0.01），SOD、GSH-Px均显著降低（P<0.01），MDA显著升高（P<0.01）；HE染色可见心肌组织水肿坏死、纤维溶解断裂；PAS染色可见大量糖原物质沉积；免疫组化示心肌组织Bax表达增多、Bcl-2表达减少（P<0.01）。与模型组比较，BXD低剂量组FPG降低（P<0.05），西药组和BXD中、高剂量组FPG均显著降低（P<0.01）；西药组HbAlc显著降低（P<0.01），BXD高剂量组HbAlc降低（P<0.05）；西药组与BXD高剂量组SOD、GSH-Px均显著升高（P<0.01）、MDA含量均降低（P<0.05）；西药组、BXD高剂量组Bax表达显著减少（P<0.01），西药组及BXD中剂量组、高剂量组Bcl-2表达显著增多（P<0.01）。结论 BXD对GK大鼠心肌损伤具有保护作用，其机制可能是通过增强抗氧化能力、抑制心肌细胞凋亡，从而起到心肌保护作用。 |
| 关键词: 糖尿病心肌病 加味生脉补心丹 GK大鼠 氧化应激 细胞凋亡 |
| DOI：10.3969/j.issn.1674-070X.2019.04.005 |
| Received:October 18, 2018 |
| 基金项目:国家自然科学基金面上项目（81373551）；中医诊断学国家重点学科开放基金（2015ZYZD03）；湖南省研究生创新课题（CX2017B428，CX2018B465） |
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| Protective Effects of Jiawei Shengmai Buxin Dan (BXD) on Myocardial Injury in Type 2 Diabetic Rats |
| WU Huaying,XIA Shuaishuai,HUANG Huiyong,PAN Jixing,LI Jing,HE Zuomei,SHAO Feng,ZENG Guang |
| (Hunan University of Chinese Medicine, Hunan Provincial Key Laboratory of Diagnostic in Chinese Medicine, Changsha, Hunan 410208, China;Changsha Traditional Chinese Medicine Hospital, Changsha, Hunan 410005, China;College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To investigate the protective effects of Jiawei Shengmai Buxin Dan (BXD) on myocardial injury in spontaneous non-obese type 2 diabetes Goto-kakisaki (GK) rats. Methods Eight male Wistar rats aged 8-9 weeks were used as a blank group. 40 diabetic GK rats were randomly divided into 5 groups:the model group, the Western medicine group (Gliclazide Sustained-release Tablets), BXD low dose group, BXD medium dose group, BXD high dose group. The rats in each group were sacrificed 10 weeks after treatment, and abdominal aortic blood sampling was used to detect fasting blood glucose (FPG), glycosylated hemoglobin (HbAlc), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA). The left ventricle was taken for myocardial tissue HE staining. PAS staining was performed to observe pathological changes. The immunohistochemistry was used determine the expression of Bax and Bcl-2 protein related to myocardial apoptosis. Results Compared with the blank group, FPG and HbAlc were significantly increased in the model group (P<0.01); SOD and GSH-Px were significantly decreased (P<0.01), and MDA was significantly increased (P<0.01); HE staining showed edema necrosis and fibrinolysis rupture in myocardial tissue; PAS staining showed a large amount of glycogen deposition; immunohistochemistry showed increased expression of Bax and decreased expression of Bcl-2 in myocardial tissue (P<0.01). Compared with the model group, the FPG of the BXD low-dose group was decreased (P<0.05), and the FPG of the western medicine group, the BXD medium and high dose group were significantly decreased (P<0.01); HbAlc in the western medicine group was significantly decreased (P<0.01), and decreased in the BXD high dose group (P<0.05). The SOD and GSH-Px in the western medicine group and the BXD high dose group were significantly increased (P<0.01) and the MDA content was decreased (P<0.05). The expression of Bax in the western medicine group and BXD high dose group was significantly decreased (P<0.01), and the expression of Bcl-2 in the western medicine group, BXD middle dose group and high dose group increased significantly (P<0.01). Conclusion BXD has protective effects on myocardial injury in GK rats. The mechanism may enhance myocardial cell apoptosis by enhancing antioxidant capacity and inhibiting cardiomyocyte apoptosis. |
| Key words: diabetic cardiomyopathy Jiawei Shengmai Buxin Dan GK rats oxidative stress apoptosis |
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