安晏 李雨杺 颜晓静

中圖分类号 R965 文献标志码 A 文章编号 1001-0408（2021）13-1572-06

DOI 10.6039/j.issn.1001-0408.2021.13.06

摘 要 目的：研究黄精多糖（PSP）对急性心肌梗死（AMI）模型大鼠心肌损伤的改善作用。方法：将大鼠按照随机数字表法分为空白对照组、模型组、阿司匹林组（阳性对照，25 mg/kg）和PSP低、中、高剂量组（0.5、1、2 g/kg），每组10只。除空白对照组外，其余大鼠均采用结扎左冠状动脉前降支以复制AMI模型。造模成功后，空白对照组和模型组大鼠灌胃生理盐水，给药组大鼠灌胃相应药物，每天1次，连续28天。末次给药后，检测大鼠左室射血分数（LVEF）、左室短轴缩短率（LVFS）;观察大鼠心肌组织病理形态学变化;采用酶联免疫吸附试验检测大鼠心肌组织中氧化应激相关指标[超氧化物歧化酶（SOD）、丙二醛（MDA）、活性氧簇（ROS）]水平;采用Western blot法检测大鼠左心室前壁组织中凋亡相关蛋白[B细胞淋巴瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）、胱天蛋白酶3（caspase-3）、caspase-8、caspase-9]和Wnt/β-联蛋白（β-catenin）通路相关蛋白（Wnt1、β-catenin）的表达水平。结果：与模型组比较，PSP中、高剂量组和阿司匹林组大鼠LVEF、LVFS和心肌组织中SOD水平以及左心室前壁组织中Bcl-2蛋白表达水平均显著升高（P<0.05）;心肌组织中MDA、ROS水平和左心室前壁组织中Bax、caspase-3、caspase-8、caspase-9、Wnt1、β-catenin蛋白表达水平均显著降低（P<0.05）;心肌组织结构紊乱和炎性细胞浸润均减轻。结论：PSP可改善AMI模型大鼠的心肌损伤;其作用机制可能与升高心肌组织中SOD水平，降低MDA、ROS水平，调控凋亡相关蛋白和Wnt/β-catenin通路相关蛋白的表达有关。

关键词 黄精多糖;急性心肌梗死;氧化应激;Wnt/β-catenin信号通路

Improvement Effects of Polygonatum sibiricum Polysaccharides on Myocardial Injury of Acute Myocardial Infarction Model Rats

AN Yan1，LI Yuxin1，YAN Xiaojing2（1. Dept. of TCM， Anyang Vocational and Technical College， Henan Anyang 455000， China; 2. Comprehensive Laboratory for Characteristic Processing Research of Menghe Clinical Prescriptions， Jiangsu Changzhou 213003， China）

ABSTRACT OBJECTIVE： To study the improvement effects of Polygonatum sibiricum polysaccharides （PSP） on the myocardial injury of acute myocardial infarction （AMI） model rats. METHODS： The rats were randomly divided into blank control group， model group， aspirin group （positive control， 25 mg/kg）， PSP low-dose， medium-dose and high-dose groups （0.5， 1， 2 g/kg）， with 10 rats in each group. Except for blank control group， AMI model was established by ligation of the anterior descending branch of the left coronary artery of rats in other groups. After modeling， blank control group and model group were given normal saline intragastrically， and administration groups were given relevant medicine intragastrically， once a day， for consecutive 28 days. After last medication， left ventricular ejection fraction （LVEF） and left ventricular short axis shorting rate （LVFS） of rats were detected. The morphological changes of myocardial tissue were observed. The levels of oxidative stress indexes （SOD， MDA， ROS） in myocardial tissue of rats were detected by ELISA. The expression of apoptosis-related proteins （Bcl-2， Bax， caspase-3， caspase-8， caspase-9） and the Wnt/β-catenin pathway-related proteins （Wnt1， β-catenin） in left ventricular anterior wall tissue of rats were detected by Western blot assay. RESULTS： Compared with model group， the levels of LVEF and LVFS， the levels of SOD in myocardial tissue and protein expression of Bcl-2 in left ventricular anterior wall tissue were increased significantly in PSP medium-dose， high-dose groups and aspirin group （P<0.05）; the levels of MDA and ROS in myocardial tissue， the protein expression of Bax， caspase-3， caspase-8， caspase-9， Wnt1 and β-catenin in left ventricular anterior wall tissue were decreased significantly （P<0.05）; myocardial tissue structure disorder and inflammatory cell infiltration were reduced. CONCLUSIONS： PSP can relieve myocardial injury in AMI model rats; its mechanism may be related to increasing SOD level in myocardial tissue， decreasing MDA and ROS level， regulating apoptosis-related proteins and Wnt/β-catenin pathway-related proteins.

KEYWORDS Polygonatum sibiricum polysaccharides; Acute myocardial infarction; Oxidative stress; Wnt/β-catenin pathway

急性心肌梗死（AMI）是一种常见的缺血性心脏病，是因冠状动脉供血急剧减少或中断导致急性缺血，从而引起严重而持续的心肌缺血性坏死[1-2]。近年来，组织工程和再生纳米医学等许多新方法被用于修复受损的心脏组织[3]，但是这些方法仍难以愈合由AMI所造成的心肌损伤。因此，寻找治疗AMI的药物具有重要意义。

在心肌梗死缺血的最初几分钟，心肌会产生强烈的氧化应激反应，进而发生心肌损伤和心肌细胞凋亡[4]。……