作　　者： (张岩）; (冯超）; (韩吉春）; (陈萌）;

机构地区： 齐河县人民医院,德州253000

出　　处： 《天然产物研究与开发》 2017年第9期1492-1497,1616,共7页

摘　　要： 研究甘草素的抗心肌缺血再灌注(I/R)损伤作用及其可能的作用机制。本研究通过Langendorff系统建立SD大鼠离体心肌I/R损伤模型,并将实验分为5组:正常组、模型组、低剂量甘草素预处理组(0.1μg/m L)、中剂量甘草素预处理组(0.5μg/m L)和高剂量甘草素预处理组(1.0μg/m L)。利用生物多导记录仪连续测定血流动力学参数。通过TTC染色检测心肌梗死面积。并用ELISA法检测冠脉流出液中肌酸激酶(CK)和乳酸脱氢酶(LDH)的活力。ELISA法检测心肌组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、白介素6(IL-6)和肿瘤坏死因子α(TNF-α)的含量。利用TUNEL法检测心肌细胞凋亡。Western blot检测心肌组织中Bax和Bcl-2的蛋白表达量。结果表明:与正常组相比较,模型组出现严重的心功能障碍和心肌梗死,冠脉流出液中LDH和CK的含量也显著升高。并且模型组心肌组织中MDA、IL-6和TNF-α含量增加,SOD的活性却显著降低。与此同时,模型组心肌细胞发生严重的凋亡现象,并且促凋亡蛋白(Bax)水平显著升高,抑制凋亡蛋白(Bcl-2)水平显著下降。与模型组对比,通过甘草素的预处理可以逆转这些I/R诱导的心肌损伤现象,并且高剂量的效果最好,呈现出一定的剂量依赖性。以上结果均表明,甘草素具有显著的抗心肌缺血再灌注损伤作用,其作用机制可能与其抗氧化、抗炎和抗凋亡作用相关。 This study evaluated the cardioprotective effects of liquiritigenin on ischemia/reperfusion （I/R） injury using an isolated Langendorff rat heart model. Adult SD rats were randomly divided into five groups ： control group, model group,low dose pretreatment group （0. 1 jjig/mL） ,middle dose pretreatment group （0. 5 jjig/mL） and high dose pre-treatment group （0. 1 jjig/mL）. The left ventricular developed pressure （LVDP） and the maximum up/down rate of the left ventricular pressure （ dp/dtmax） were documented as the indices of myocardial function by a physiological recorder. TTC staining was performed to assess infarct size. Coronary effluent was analyzed for lactate dehydrogenase （LDH） and creatine kinase （CK） release to assess the degree of cardiac injury. Superoxide dismutase （SOD） activity and malondi- aldehyde （MDA） level were analyzed to determine the oxidative stress status of myocardial tissue. The levels of tumor necrosis factor-（TNF-） and interleukin-6 （IL-6） were analyzed to determine the inflammation status of myocardial tis-sue. Cardiomyocyte apoptosis analysis was performed using an TUNEL Kit. The proteins levels of Bax and Bcl-2 were measured by Western blot. The results showed that liquiritigenin （0.5 and 1.0 jjig/mL） pretreatment decreased CK and LDH levels in coronary flow,and attenuated myocardial infarct size. This pretreatment with liquiritigenin also increased SOD activity,but decreased MDA,TNF-a and IL-6 activities. The cell apoptosis in the hearts from the liquiritigenin-trea-ted group were lower than those in the hearts from the model group. Meanwhile, the expression levels of bcl-2 expression was upregulated, the expression levels of bax was downregulated. Therefore, the cardioprotective effects of liquiritigenin m a y beattributed to its antioxidant,anti-inflammatory and anti-apoptosis activities.

关 键 词： 甘草素 心脏保护 抗氧化 抗炎 抗凋亡