虎杖苷对糖尿病小鼠心肌纤维化的保护作用及机制  

Effect of polydatin on myocardial fibrosis in STZ-induced diabetic mice

作　　者：陈瑞敏 陈伟 李建耿 李宁 谈红 CHEN Ruimin;CHEN Wei;LI Jiangeng;LI Ning;TAN Hong(Department of Cardiology,the 960th Hospital of the Joint Logistic Support Force of the Chinese People's Liberation Army,Jinan 250031,China;不详)

机构地区：[1]解放军联勤保障部队第九六〇医院心内科,济南250031 [2]山东第一医科大学第三附属医院心内科

出　　处：《山东医药》2021年第22期47-50,共4页Shandong Medical Journal

摘　　要：目的探讨虎杖苷对糖尿病小鼠心肌纤维化的影响,并阐明其作用机制。方法取32只雄性C57小鼠,随机取8只作为正常对照组,其余24只制作糖尿病模型。采用链脲佐菌素(STZ)诱导,以60μg/g剂量一次性腹腔注射制备糖尿病模型。将糖尿病小鼠分为三组,虎杖苷低剂量组、虎杖苷高剂量组分别给予虎杖苷100、200 mg/(kg.d)灌胃给药,糖尿病组给予等体积溶剂。给药12周后检测各组小鼠心脏质量指数、血糖水平,并检测心功能指标(E/A、LVEF、FS)。天狼星红、Masson染色测定心肌胶原纤维表达,免疫组化法检测各组小鼠心肌组织中的胶原水平,Western blotting法检测各组小鼠心肌组织中胶原Ⅰ、Ⅲ、转化生长因子-β1(TGF-β1)、Smad3、α-平滑肌肌钙蛋白(α-SMA)、纤维连接蛋白(FN)蛋白表达。结果与正常对照组比较,糖尿病组小鼠血糖水平、胶原、TGF-β1、Smad3、α-SMA、FN蛋白升高,纤维化损伤加重,E/A、LVEF、FS下降(P均<0.05),心脏收缩舒张功能受损;与糖尿病组相比,虎杖苷低剂量组、高剂量组E/A、LVEF、FS升高(P均<0.05),胶原、TGF-β1、Smad3、α-SMA降低(P均<0.05)。结论虎杖苷能减轻糖尿病小鼠心肌纤维化,其机制可能与抑制TGF-β1/Smad3、降低胶原表达有关。Objective To study the protective effect of polydatin on STZ-induced diabetic mice with myocardial fi‐brosis and to clarify the mechanism.Methods Streptozotocin(STZ)-induced diabetic mice were randomly divided into the diabetes group,low-dose polydatin group(100 mg/kg/d),high-dose polydatin group(200 mg/kg.d),and normal control group.After 12 weeks of administration,cardiac mass index,blood glucose level and cardiac function indexes(E/A,LVEF,and FS)were detected.Sirius red and Masson staining were used to detect the expression of myocardial colla‐gen fibers,immunohistochemistry was used to detect the level of collagen in the myocardial tissues,and Western blotting was used to detect collagen I,III,and transforming growth factor-β1(TGF-β1),Smad3,α-smooth muscle troponin(α-SMA),and fibronectin(FN)protein expression in the myocardial tissues.Results Compared with the normal control group,the blood sugar level,collagen and TGF-β1,Smad3,α-SMA,and FN protein increased,and the fibrosis injury was aggravated,E/A,LVEF,and FS decreased,the cardiac systolic and diastolic functions were impaired in the diabetic group(all P<0.05).After the intervention of polydatin,the above effects were relieved and the myocardial damage of dia‐betic mice was alleviated.Conclusion Polydatin attenuates the myocardial fibrosis and improves cardiac function in STZ-induced diabetic mice by inhibiting TGF-β1/Smad3 and the expression of collagen.

关 键 词：糖尿病 心肌纤维化 虎杖苷 转化生长因子Β1 SMAD3 

分 类 号：R587.1[医药卫生—内分泌]