CAJ | 학술논문

目的：探讨仙茅多糖（ COP）对阿霉素（ ADM）诱导小鼠中毒性心肌损伤的保护作用及其机制。方法选用ADM建立小鼠心肌损伤模型。测定血清肌酸激酶（CK）、乳酸脱氢酶（LDH）、谷草转氨酶（GOT）和一氧化氮合酶（NOS）、超氧化物歧化酶（SOD）活力、丙二醛（MDA）含量、心肌SOD、MDA等生化指标，并观察心肌结构变化。结果 ADM可致血清CK、LDH、GOT和 NOS活力升高（ P＜0．01），同时血清和心肌SOD活力下降而MDA含量升高（P＜0．01）。 COP能降低血清CK、LDH、GOT和NOS活力（P＜0．05或 P＜0．01），增加心肌SOD活力和降低MDA含量（P＜0．05或P＜0．01）。光镜也证实了COP的保护作用。结论 COP对ADM引起的心肌损伤具有明显保护作用，其作用机制可能与抗自由基、抑制脂质过氧化作用有关。
목적：탐토선모다당（ COP）대아매소（ ADM）유도소서중독성심기손상적보호작용급기궤제。방법선용ADM건립소서심기손상모형。측정혈청기산격매（CK）、유산탈경매（LDH）、곡초전안매（GOT）화일양화담합매（NOS）、초양화물기화매（SOD）활력、병이철（MDA）함량、심기SOD、MDA등생화지표，병관찰심기결구변화。결과 ADM가치혈청CK、LDH、GOT화 NOS활력승고（ P＜0．01），동시혈청화심기SOD활력하강이MDA함량승고（P＜0．01）。 COP능강저혈청CK、LDH、GOT화NOS활력（P＜0．05혹 P＜0．01），증가심기SOD활력화강저MDA함량（P＜0．05혹P＜0．01）。광경야증실료COP적보호작용。결론 COP대ADM인기적심기손상구유명현보호작용，기작용궤제가능여항자유기、억제지질과양화작용유관。
Objective To study the protective effects and its mechanisms of Common Curculigo Rhizome polysaccharide ( COP) on adriamycin ( ADM)-induced cardiotoxicity in mice .Methods ADM was injected to induce myocardium injury model in mice .The activities of several serum enzymes were measured ,including the activities of creatine kinase ( CK) ,lactate dehydrogenase ( LDH) ,glutamic-oxaloace-tic transaminase ( GOT) ,Nitric-oxide synthase ( NOS) ,superoxide dismutase ( SOD).The serous and myocardial malondialdehyde ( MDA) contents and the myocardial SOD activities were detected .The pathological lesion of myocardium was observed .Results ADM induced se-vere myocardial damages with the increasing activities of serous CK ,LDH,GOT and NOS (P<0.01).ADM decreased serous and myocardial SOD activities,while increased the MDA content (P<0.01).The activities of serous CK,LDH,GOT,NOS in COP group were decreased compared with those of ADM group (P<0.05 or P<0.01) and myocardial SOD activities was increased ,MDA content was decreased (P<0.05 or P<0.01).The changes of myocardial pathological damages were improved by light microscope .Conclusions COP shows signifi-cant protective effects on myocardial damage induced by ADM .The mechanism might be related to the effects of anti-free radical and the in-hibition of lipid peroxidation .