CAJ | 학술논문

目的：观察加参方对大鼠心梗早期梗死范围、心功能以及心肌中炎症因子产生的影响。方法：采用结扎左冠状动脉前降支的方法制作急性心梗大鼠模型，将Sprague-Dawley（SD）大鼠随机分成5组：假手术组、模型组、加参方3 g（3 g·kg-1·day-1）组、加参方6 g（6 g·kg-1·day-1）组和氯沙坦（10 mg·kg-1·day-1）组。于心梗后第3天应用伊文氏蓝和2，3，5-氯化三苯基四氮唑（TTC）双染色法测定大鼠心肌梗死范围，并于心梗后第7天应用超声心动图和酶联免疫吸附法（ELISA）分别观察和测定大鼠心脏结构和收缩功能，以及缺血心肌中肿瘤坏死因子α（TNF-α）、白介素1β（IL-1β）和单核细胞趋化蛋白1（MCP-1）的含量变化。结果：与模型组相比，加参方6 g组梗死范围明显缩小（P<0.05），左室舒张末直径（LVEDD）和左室收缩末直径（LVESD）明显减小（P<0.05），左室射血分数（LVEF）和左室短轴缩短率（LVFS）明显增加（P<0.05），其结果与氯沙坦组相似。与模型组相比，加参方可明显降低心肌组织中TNF-α、IL-1β和MCP-1的产生（P<0.05），除TNF-α外，该作用呈剂量依赖性。其中加参方6 g的作用与氯沙坦相似。结论：加参方可缩小心肌梗死范围，改善心脏功能，同时降低缺血心肌中炎症介质的表达，该作用与氯沙坦相似，提示在心梗早期加参方具有保护心脏、抑制炎症的作用，其中保护心脏的作用可能是通过对炎症反应的抑制来实现。
목적：관찰가삼방대대서심경조기경사범위、심공능이급심기중염증인자산생적영향。방법：채용결찰좌관상동맥전강지적방법제작급성심경대서모형，장Sprague-Dawley（SD）대서수궤분성5조：가수술조、모형조、가삼방3 g（3 g·kg-1·day-1）조、가삼방6 g（6 g·kg-1·day-1）조화록사탄（10 mg·kg-1·day-1）조。우심경후제3천응용이문씨람화2，3，5-록화삼분기사담서（TTC）쌍염색법측정대서심기경사범위，병우심경후제7천응용초성심동도화매련면역흡부법（ELISA）분별관찰화측정대서심장결구화수축공능，이급결혈심기중종류배사인자α（TNF-α）、백개소1β（IL-1β）화단핵세포추화단백1（MCP-1）적함량변화。결과：여모형조상비，가삼방6 g조경사범위명현축소（P<0.05），좌실서장말직경（LVEDD）화좌실수축말직경（LVESD）명현감소（P<0.05），좌실사혈분수（LVEF）화좌실단축축단솔（LVFS）명현증가（P<0.05），기결과여록사탄조상사。여모형조상비，가삼방가명현강저심기조직중TNF-α、IL-1β화MCP-1적산생（P<0.05），제TNF-α외，해작용정제량의뢰성。기중가삼방6 g적작용여록사탄상사。결론：가삼방가축소심기경사범위，개선심장공능，동시강저결혈심기중염증개질적표체，해작용여록사탄상사，제시재심경조기가삼방구유보호심장、억제염증적작용，기중보호심장적작용가능시통과대염증반응적억제래실현。
This article was aimed to determine effects of Jia-Shen prescription (JSP) on infarct size (IS), cardiac function and myocardial cytokine in the early phase of myocardial infarction (MI) in rats. Acute MI models were induced by the ligation of left anterior descending coronary artery in Sprague-Dawley (SD) rats. The rats were ran-domly divided into five groups, which were the sham-operated group, model group, JSP-3 g (3 g·kg-1·day-1) group, JSP-6 g (6 g·kg-1·day-1) group, and the losartan (10 mg·kg-1·day-1) group. IS was determined by Evans blue and 2,3,5-Triphenyltetrazolium chloride (TTC) 3 days after MI. The left ventricular structure and contractility were measured by echocardiography performed 7 days after MI. And contents of myocardial inflammatory mediators in-cluding tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and monocyte chemoattractant protein-1 (MCP-1) were measured by ELISA. The results showed that compared with the model group, treatment with JSP at the dose of 6 g significantly reduced myocardial IS (P<0.05);left ventricular end diastolic diameter (LVEDD) and left ventricu-lar end systolic diameter (LVESD) were significantly decreased (P<0.05); left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly increased (P<0.05).The results were similar as the losartan group. Compared with the model group, JSP can significantly reduce the production of TNF-α, IL-1βand MCP-1 in cardiac tissues (P<0.05). Except TNF-α, these effects of JSP were in a dose-dependent manner. JSP (6 g) had equal effectiveness with losartan. It was concluded that consistent with losartan-induced cardioprotection, JSP administered after MI reduced myocardial IS, improved cardiac function, and decreased inflammatory mediators in ischemic myocardium. The data indicated that JSP exerted its cardioprotection possibly via inhibiting inflammatory response.