Galectin-3拮抗剂——MCP对缺血性心功能不全的作用

发布时间：2018-05-07 07:19

  本文选题：半乳糖凝聚素- + 改良的柑橘果胶　； 参考：《临床心血管病杂志》2017年06期

【摘要】：目的:通过galectin-3(gal-3)抑制剂——改良的柑橘果胶(modified citrus pectin,MCP)治疗心肌梗死后心功能不全家兔,探讨MCP对缺血性心功能不全的治疗作用。方法:(1)30只家兔随机分为假手术组、心功能不全组、MCP组;(2)结扎冠状动脉前降支制作家兔心肌梗死后心功能不全模型,心功能不全模型制作成功后,MCP组予75mg/ml MCP(2ml·kg-1·d-1)、假手术组及心功能不全组予0.9%氯化钠溶液(2ml·kg-1·d-1)各灌胃4周;(3)心脏超声仪、ELISA法分别检测家兔术前及术后2、4、6周心功能及血清gal-3表达情况;(4)RT-PCR和WesternBlot分析心肌梗死边缘区gal-3、胶原蛋白Ⅰ、胶原蛋白ⅢmRNA和蛋白表达水平,并计算胶原蛋白Ⅰ/Ⅲ比值;(5)给药4周后取各组心肌梗死边缘区组织,用Masson法胶原染色分析心肌梗死边缘区纤维化。结果:(1)给药2周、4周后MCP组心功能较心功能不全组明显好转(P0.01);(2)给药2周、4周后心功能不全组血清gal-3浓度远远高于MCP组(P0.05);(3)给药4周后心功能不全组梗死边缘区gal-3、胶原蛋白Ⅰ、胶原蛋白Ⅲ的mRNA表达较MCP组均明显增高(P0.01);(4)光学显微镜下心功能不全组可见心肌细胞排列紊乱,部分心肌细胞坏死、水肿、肥大,心肌纤维增粗。小血管壁增厚并可见周围有大量蓝绿色胶原纤维增生并包绕分割心肌细胞,心肌间质纤维增生、胶原大量沉积并伴有炎性细胞浸润;(5)心功能不全组中梗死边缘区域心肌组织gal-3、胶原蛋白Ⅰ、胶原蛋白Ⅲ蛋白表达明显高于MCP组和假手术组。结论:在心功能不全家兔中,gal-3表达的增加与心脏功能不全、纤维化、心肌胶原蛋白大量沉积有关,但是通过MCP可以阻止gal-3的表达,改善心肌梗死边缘区域的纤维化程度。gal-3在心室重构和其引起的功能障碍中起到关键的作用,gal-3或许可作为治疗心力衰竭新的靶点。
[Abstract]:Aim: to study the therapeutic effect of MCP on ischemic cardiac dysfunction in rabbits with myocardial infarction by modified citrus pectinus (citrus), a galectin-3gal-3 inhibitor. Methods Thirty rabbits were randomly divided into sham-operation group (MCP group) and MCP group (2) ligation of anterior descending branch of coronary artery to make the model of cardiac insufficiency after myocardial infarction in rabbits. After successful cardiac insufficiency model, 75mg/ml MCP(2ml kg-1 d-1 was given to MCP group, 0.9% sodium chloride solution was given to 2 ml kg-1 d-1 in sham operation group and cardiac insufficiency group was given 0.9% sodium chloride solution for 4 weeks. The cardiac function and serum gal-3 were measured by Elisa before operation and 2 weeks after operation by using hypersonic enzyme linked immunosorbent assay (Elisa). RT-PCR and WesternBlot were used to analyze gal-3, collagen 鈪，

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