Fan Yunlong, Jin Linjing, Wu Yue, Fan Yanming, Wei Qingmin
Department of Cardiology, Xingtai People's Hospital Xingtai 054001, Hebei Province, China.
Department of Internal Medicine, Xingtai Hospital of Traditional Chinese Medicine Xingtai 054001, Hebei Province, China.
Am J Transl Res. 2021 Apr 15;13(4):2518-2527. eCollection 2021.
This study was designed to observe the effects of metoprolol on serum inflammatory factors, cardiac function and oxidative stress response in rats modeled with coronary heart disease (CHD).
Thirty clean SD rats aged 6-8 weeks were randomized into a control group (CG), treatment group (TG) and model group (MG), with 10 in each group. Rats in the CG were fed regular chow, while those in the MG and TG were fed a high-fat diet. After successful CHD modeling, those in the TG were given metoprolol every day, 10 mg/kg once a day. The effects of cardiac function indexes, myocardial injury indexes, blood lipids, inflammatory factors and oxidative stress indexes, myocardial apoptosis-related factors and apoptosis rate were observed and recorded before and after treatment.
Compared with the CG, the cardiac function indexes of the MG decreased significantly, while the myocardial injury indexes increased markedly. After metoprolol treatment, the cardiac function and myocardial injury of the TG were significantly improved. Also, the expression of serum lipid indexes in the MG increased obviously, and the hyperlipidemia in the TG was improved after metoprolol treatment. Besides, the expression of inflammatory factors in serum of the MG increased remarkably, and metoprolol could reduce the inflammatory state in rats. Furthermore, MDA in serum of the MG increased, SOD, CAT, GSH-Px decreased; revealing that metoprolol can improve oxidative stress in rats. Finally, the apoptosis rate of cardiomyocytes in the MG increased dramatically. Metoprolol treatment can reduce the apoptosis rate and improve the expression of apoptosis related proteins.
Metoprolol reduces the degree of myocardial injury, inhibits inflammatory reaction and oxidative stress , reduces myocardial apoptosis and improves myocardial ischemia in CHD modeled rats.
本研究旨在观察美托洛尔对冠心病（CHD）模型大鼠血清炎症因子、心功能及氧化应激反应的影响。
将30只6 - 8周龄的清洁级SD大鼠随机分为对照组（CG）、治疗组（TG）和模型组（MG），每组10只。CG组大鼠给予常规饲料，MG组和TG组大鼠给予高脂饮食。成功建立CHD模型后，TG组大鼠每天给予美托洛尔，剂量为10 mg/kg，每日1次。观察并记录治疗前后心功能指标、心肌损伤指标、血脂、炎症因子及氧化应激指标、心肌凋亡相关因子及凋亡率的变化。
与CG组相比，MG组心功能指标显著降低，心肌损伤指标明显升高。美托洛尔治疗后，TG组的心功能和心肌损伤得到显著改善。此外，MG组血清脂质指标表达明显升高，美托洛尔治疗后TG组高脂血症得到改善。另外，MG组血清炎症因子表达显著增加，美托洛尔可减轻大鼠的炎症状态。再者，MG组血清丙二醛（MDA）升高，超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH - Px）降低；表明美托洛尔可改善大鼠氧化应激。最后，MG组心肌细胞凋亡率显著升高。美托洛尔治疗可降低凋亡率并改善凋亡相关蛋白的表达。
美托洛尔可减轻CHD模型大鼠的心肌损伤程度，抑制炎症反应和氧化应激，减少心肌凋亡，改善心肌缺血。
