CAJ | 학술논문

目的研究益气活血中药复方对CVB3乳鼠心肌细胞感染模型线粒体核糖体蛋白L51(mitochondrial ribosomal protein L51,MRPL51)表达的影响,以期从基因水平揭示CVB3心肌炎的发病机制及益气活血中药复方治疗病毒性心肌炎的作用机制,并进一步证实益气活血中药复方治疗CVB3病毒性心肌炎的有效性.方法通过乳鼠心肌细胞培养,建立病毒组和益气活血中药复方组心肌细胞模型,以改良的抑制性消减杂交技术(suppression subtractive hybridization,SSH),分离两组差异表达的基因,并通过荧光RT-PCR对上述结果进行验证.结果 SSH结果显示,MRPL51基因在益气活血中药复方组为低表达,而在病毒组则呈高表达状态,荧光RT-PCR结果显示益气活血中药复方组中MRRPL51基因达到阈值的循环数(Ct)明显多于病毒组,提示MRPL51在病毒组中的表达较中药组中高.结论 MRPL5基因表达上调可能是CVB3致病毒性心肌炎机制之一;益气活血中药复方通过下调MRPL5基因的表达而实现治疗病毒性心肌炎的目的 .
목적 연구익기활혈중약복방대CVB3유서심기세포감염모형선립체핵당체단백L51(mitochondrial ribosomal protein L51,MRPL51)표체적영향,이기종기인수평게시CVB3심기염적발병궤제급익기활혈중약복방치료병독성심기염적작용궤제,병진일보증실익기활혈중약복방치료CVB3병독성심기염적유효성.방법 통과유서심기세포배양,건립병독조화익기활혈중약복방조심기세포모형,이개량적억제성소감잡교기술(suppression subtractive hybridization,SSH),분리량조차이표체적기인,병통과형광RT-PCR대상술결과진행험증.결과 SSH결과현시,MRPL51기인재익기활혈중약복방조위저표체,이재병독조칙정고표체상태,형광RT-PCR결과현시익기활혈중약복방조중MRRPL51기인체도역치적순배수(Ct)명현다우병독조,제시MRPL51재병독조중적표체교중약조중고.결론 MRPL5기인표체상조가능시CVB3치병독성심기염궤제지일;익기활혈중약복방통과하조MRPL5기인적표체이실현치료병독성심기염적목적 .
Objective To study the effects of the recipe for activating blood circulation and nourishing qi on expression of mitochondrial ribosomal protein L51 (MRPL51) in CVB3 infection model in rat cardiac myocytes, to reveal the pathogenesis of CVB3 myocarditis in the genetic level, to explore the therapeutic mechanism of the recipe for activating blood circulation and nourishing qi on CVB3 myocarditis, and to confirm the validity of the recipe for activating blood circulation and nourishing qi on CVB3 myocarditis. Methods After establishing CVB3 infection model and treatment model with recipe for activating blood circulation and nourishing qi by culturing neonatal rat myocardial cells, a modified suppression subtractive hybridization (SSH) was used to isolate differentially expressed genes between two model groups. These results were further verified by fluorescence RT-PCR. Results The results of SSH showed that gene expression of the treatment group was lower than that of the CVB3 infection group. The results of fluorescent RT-PCR which agreed with that of SSH displayed the threshold cycle number (Ct) in the treatment group was higher than the virus group. Conclusion Up-regulation of MRPL51 might be one of the pathogenesis of CVB3 myocarditis. The recipe for activating blood circulation and nourishing qi could treat viral myocarditis by regulating the expression of MRPL51.