中文摘要：

目的观察串珠素参与碱性成纤维细胞生长因子对于缺血心肌的保护。方法大鼠心肌梗死模型建立后，随机分为碱性成纤维细胞生长因子（bFGF）＋心肌缺血（MI）组（bFGF＋MI组，缺血边缘区注射bFGF）、MI组（缺血边缘区注射等体积生理盐水）和假手术组（sham组）。分别于梗后24h、14d、28d结束实验。检测血流动力学参数，红四氮唑法测定心肌梗死面积，免疫组化法计数微血管数目，实时定量PCR检测串珠素mRNA表达，Western印迹检测FAK、P—p38MAPK变化。结果缺血区边缘注射hFGF后，心肌功能改善，心梗面积较MI组减小，微血管数目增加，多于MI组，串珠素mRNA在缺血边缘区、梗区表达增加，FAK、P—p38表达上调。结论bFGF明显改善大鼠急性心肌梗死后心肌功能，缩小梗死面积，促进缺血心肌血管新生，串珠素参与bFGF对于缺血心肌的保护，其细胞信号转导机制涉及FAK的激活和p38MAPK信号转导途径。

英文摘要：

Objective To investigate ff pedecan （PN） is involved in the myocardial protection of basic fibroblast growth factor （bFGF） in acute myocardial infarction. Methods Twenty-four Wistar rats were randomized into 3 groups ： myocardial infarction group （ MI group, n = 8, undergoing ligation of the descending anterior branch of the left coronary artery） , bFGF ＋ MI group （ n = 10, injected with bFGF into the border myocardium between the infracted and non- infracted areas immediately after the ligation of the descending anterior branch）, and sham operation group （n = 6, undergoing sham operation and injection of normal saline）. 24 h, 14 days, and 28 days after the operation the hemodynamic parameters, infarct size, and microvessel density （MVD） were observed. The hearts were taken out, RT-PCR was used to detect the mRNA expression of PN, and Western blotting was used to detect the expression of focal adhesion kinase （FAK） and p38 mitogen-activated protein kinase （MAPK） phosphorylation. Results In the bFGF ＋ MI group, the ＋ dp/dt and - dp/dt were improved markedly, the infarct size was significantly smaller, the MVD value was higher than those of the MI group on day 14 and day 28 ; the perlecan mRNA expression was higher in the infarct marginal area and interior zone; and the expression of FAK and the p38MAPK phosphorylation were up-regulated in the marginal zone of the bFGF group. Conclusion bFGF is useful in promoting ischemic myocardial angiogenesis; reducing the size of infracted myocardium, and improving the ventricular function in acute myocardial infarction. Perlecan participates in the cardiac protection induced by bFGF. The relevant pathway is related to up-regulation of FAK and p38MAPK.