CAJ | 학술논문

目的：探讨右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及其机制，为临床用药提供实验依据。方法将35只 SD 大鼠随机分为5组：正常对照组、模型组（表柔比星+生理盐水）、表柔比星+低剂量右丙亚胺组（DEX1）、表柔比星+中剂量右丙亚胺组（DEX2）、表柔比星+高剂量右丙亚胺组（DEX3），给药后检测各组大鼠心肌组织微量丙二醛（MDA）含量、总超氧化物歧化酶（T-SOD）活性和血浆乳酸脱氢酶（LDH）水平并观察心肌细胞凋亡的情况。结果与正常对照组比较，模型组大鼠心肌组织的 SOD 活性明显降低，MDA 含量、血浆 LDH 含量和心肌细胞凋亡指数均明显升高（P<0.01）；而与模型组比较，用右丙亚胺处理的各组大鼠心肌组织 SOD 活性明显升高，心肌组织 MDA 含量、心肌细胞凋亡指数及血浆 LDH 含量均显著降低（P<0.01或 P<0.05）。结论右丙亚胺能减少表柔比星所致的心肌细胞凋亡，可能与其降低氧自由基的产生和脂质过氧化产物含量有关。
목적：탐토우병아알대표유비성치대서심기손상적보호작용급기궤제，위림상용약제공실험의거。방법장35지 SD 대서수궤분위5조：정상대조조、모형조（표유비성+생리염수）、표유비성+저제량우병아알조（DEX1）、표유비성+중제량우병아알조（DEX2）、표유비성+고제량우병아알조（DEX3），급약후검측각조대서심기조직미량병이철（MDA）함량、총초양화물기화매（T-SOD）활성화혈장유산탈경매（LDH）수평병관찰심기세포조망적정황。결과여정상대조조비교，모형조대서심기조직적 SOD 활성명현강저，MDA 함량、혈장 LDH 함량화심기세포조망지수균명현승고（P<0.01）；이여모형조비교，용우병아알처리적각조대서심기조직 SOD 활성명현승고，심기조직 MDA 함량、심기세포조망지수급혈장 LDH 함량균현저강저（P<0.01혹 P<0.05）。결론우병아알능감소표유비성소치적심기세포조망，가능여기강저양자유기적산생화지질과양화산물함량유관。
Objective To explore the effects of dexrazoxane on pharmorubicin induced myocardial damage and its mecha-nisms. Methods 35 SD rats were randomly divided into five groups: control group, model group (epirubicin+saline); DEX1 group (epirubicin+low dose of dexrazoxane); DEX2 group (epirubicin+medium dose of dexrazoxane); DEX3 group (epirubicin+high dose of dexrazoxane). After administration, we detected the malondialdehyde (MDA) content and total superoxide dismutase (T-SOD) activity in myocardial tissues, plasma lactate dehydrogenase (LDH) levels of each group, and observed cardiomyocyte apoptosis in all groups. Results Compared with the control group, the SOD activity in myocardial tissue of model group was sig-nificantly decreased, and the MDA content in myocardial tissue, the plasma LDH content, and myocardial cell apoptotic index were significantly increased (P<0.01). Compared with the model group, the SOD activity in myocardial tissue of rats treated by different doses of dexrazoxane was markedly increased, and the MDA content in myocardial tissue, the plasma LDH content, and myocardial cell apoptotic index were significantly decreased (P<0.01 or P<0.05). Conclusion Dexrazoxane could relieve pharmorubicin-induced myocardial apoptosis. This may be associated with that it could reduce the produce of oxygen radical and lipid peroxidation.