CAJ | 학술논문

目的：观察缩醛基毛冬青提取化合物 R4对在体大鼠急性心肌缺血/再灌注损伤（ I/R）的影响，并探讨其保护作用机制。方法建立大鼠心肌缺血/再灌注模型，采用试剂盒测定再灌注40 m in后血清肌酸激酶（CK）、肿瘤坏死因子（TNF α）、IL 1Β的水平，观察心肌梗死范围，采用凝胶电泳法测定核转录因子κB（NF κB）的活性，采用试剂盒测定测定心肌组织超氧化物（ SOD）活性及丙二醛（MDA）含量。结果缺血20 m in再灌注40 m in后模型组及用药组的血清 TNF α、IL 1β、CK水平明显高于假手术组，且缩醛基毛冬青提取化合物 R 4组及维拉帕米对照组明显低于模型组。再灌注40m in后模型组及用药组的梗死范围明显增加， NF κB表达明显增高，且缩醛基毛冬青提取化合物 R4组及维拉帕米对照组明显低于模型组。再灌注40 m in后模型组及用药组的SOD明显降低，MDA明显增高，缩醛基毛冬青提取化合物 R4组及维拉帕米对照组 MDA明显低于模型组，SOD明显高于模型组，有统计学意义。结论缩醛基毛冬青提取化合物 R4对缺血再灌注心肌的保护作用与其显著缩小心肌梗死面积，降低肌酸磷酸激酶，降低 MDA同时提高 SOD ，减少心肌细胞内 TNF α、IL 1β、NF κB蛋白的表达有关。
목적：관찰축철기모동청제취화합물 R4대재체대서급성심기결혈/재관주손상（ I/R）적영향，병탐토기보호작용궤제。방법건립대서심기결혈/재관주모형，채용시제합측정재관주40 m in후혈청기산격매（CK）、종류배사인자（TNF α）、IL 1Β적수평，관찰심기경사범위，채용응효전영법측정핵전록인자κB（NF κB）적활성，채용시제합측정측정심기조직초양화물（ SOD）활성급병이철（MDA）함량。결과결혈20 m in재관주40 m in후모형조급용약조적혈청 TNF α、IL 1β、CK수평명현고우가수술조，차축철기모동청제취화합물 R 4조급유랍파미대조조명현저우모형조。재관주40m in후모형조급용약조적경사범위명현증가， NF κB표체명현증고，차축철기모동청제취화합물 R4조급유랍파미대조조명현저우모형조。재관주40 m in후모형조급용약조적SOD명현강저，MDA명현증고，축철기모동청제취화합물 R4조급유랍파미대조조 MDA명현저우모형조，SOD명현고우모형조，유통계학의의。결론축철기모동청제취화합물 R4대결혈재관주심기적보호작용여기현저축소심기경사면적，강저기산린산격매，강저 MDA동시제고 SOD ，감소심기세포내 TNF α、IL 1β、NF κB단백적표체유관。
O bjective To study the effect o fMDQR4 on acute m yocardia l ischem ia reperfusion( I/R) in rats. Methods M anufac-ture the m ode l o fm yocardia l I/R in rats. U sing kit to observe the leve ls o f serum crea tine kinase(CK) ,tum o r necrosis facto r a lpha (TNF α) and interleukin 1β( IL 1β). and the infarct size o f each group w ere m easured by TTC sta ining. And the leve l o f NF κB w as a lso de tected.And contento fm a londia ldehyde(MDA) and superoxide dism utase(SOD) in m yocardia l tissue w ere observed. Re-sults Fo low ing ischem ia 20m in and reperfusion 40m in,serum concentra tion o f TNF α ,IL 1β and CK in I/R group and m edicine pre trea tm ent group w as significantly increased com pared w ith tha t in sham group,and serum concentra tion o fTNF α ,IL 1β and CK in every m edicine pre trea tm ent group w as significantly low er than tha t in I/R group. Fo low ing ischem ia 20 m in and reperfusion 40 m in,infarct size and the expression o fNF κB in I/R group and m edicine pre trea tm ent group w as significantly increased. And infarct size and the expression o f NF κB in every m edicine pre trea tm ent group w as significantly low er than tha t in I/R group. Fo low ing reperfusion 40m in ,MDA contentw as significantly increased and SOD contentw as significantly reduced com pared w ith tha t in sham group,and MDA content in every m edicine pre trea tm ent group w as significantly low er than tha t in I/R group ,and SOD content in ev-ery m edicine pre trea tm ent group w as significantly higher than tha t in I/R group. Conclusion MDQR4 could reduce the infarct size and inhibitNF κB activa tion and dow n regula te the expression o f TNF α ,IL 1β ,CK ,MDA and increase the content o f SOD ,w hich m ay be one o f the m echanism s o f its cardiopro tection.