CAJ | 학술논문

目的：探讨丹七片干预心肌缺血的作用机制。方法缩窄环法制备小型猪心肌缺血模型，给予丹七片每次9 g /（只?天）临床等效剂量，4周。双向凝胶电泳质谱联用法分析血浆蛋白表达谱变化。结果与模型组比较，丹七片下调蛋白点9个（丰度比值≤0．5）、上调蛋白点11个（比值≥1．5）。鉴定出的上调蛋白为载脂蛋白 A1和载脂蛋白 E。结论通过上调载脂蛋白 A1和载脂蛋白 E抑制缺血心肌过度的炎症反应，可能是丹七片干预心肌缺血的主要机制之一。
목적：탐토단칠편간예심기결혈적작용궤제。방법축착배법제비소형저심기결혈모형，급여단칠편매차9 g /（지?천）림상등효제량，4주。쌍향응효전영질보련용법분석혈장단백표체보변화。결과여모형조비교，단칠편하조단백점9개（봉도비치≤0．5）、상조단백점11개（비치≥1．5）。감정출적상조단백위재지단백 A1화재지단백 E。결론통과상조재지단백 A1화재지단백 E억제결혈심기과도적염증반응，가능시단칠편간예심기결혈적주요궤제지일。
Objective To explore the effect of Danqi table t(DQT) on plasma proteome in sw ines w ith myocardial ischem ia. Me thods Myocardial ischem ia was induced by a constrictoron the left coronary artery.After treated by DQT w ith a dose of 9 g per day for4 weeks ,two dimension e lectrophoresis andmass spectrome terwas used to analyze the changes ofplasma proteome .Re-sults The abundances of 9 prote in spots were decreased while 11 prote in spots increased in animals treated by DQT.Apolipopro-te in A1 and apolipoprote in E were identified as increased prote ins .Conclusion DQTmay negative ly regulate the excess inflamma-tion induced by myocardial ischem ia and it is proved by increase plasma apolipoprote in A1 and apoliopoprote in E.