目的：探讨参麦注射液对糖尿病心肌病心肌纤维化的干预作用并初步探讨其机制。方法：将30只Wistar大鼠分为对照组、糖尿病组以及治疗组，每组各10只。采用链脲佐菌素单次腹腔注射的方法制作大鼠糖尿病模型，以枸橼酸缓冲液腹腔注射为对照，治疗组则采用腹腔注射的方式给予参麦注射液干预治疗。采用心室插管对大鼠心功能进行评估；Masson染色观察大鼠心脏组织中胶原水平；二氢乙啶染色观察大鼠心脏组织中活性氧（ROS）水平；Western blotting观察大鼠心肌组织中I型胶原、基质金属蛋白酶2（MMP-2）以及金属蛋白酶组织抑制剂2（TIMP-2）的表达水平。结果：与对照组相比，糖尿病组心功能显著下降（P＜0．05）；而治疗组心功能则显著恢复（P＜0．05）。与对照组相比，糖尿病组心肌组织ROS及胶原生成水平显著升高（P＜0．05），但经参麦注射液治疗后均显著降低（P＜0．05）。与对照组相比，糖尿病组I型胶原及TIMP-2表达水平显著升高（P＜0．05），而MMP-2水平显著降低（P＜0．05）；与糖尿病组相比，治疗组I型胶原及TIMP-2水平显著降低（P＜0．05），而MMP-2水平则显著升高（P＜0．05）。结论：参麦注射液可能通过抑制氧化应激损伤而减轻糖尿病心肌病心肌纤维化程度。%AIM:To explore the effects of Shenmai injection on myocardial fibrosis in a rat model of diabetic cardiomyopathy (DCM).METHODS:Wistar rats (n=30) were randomly divided into control group , diabetes group and treatment group.Single intraperitoneal injection of streptozotocin was utilized to establish a rat model of DCM .The rats with DCM in treatment group were intraperitoneally injected with Shenmai injection .Ventricular cannulation was applied to as-sess the cardiac functions.The formation of collagen in the cardiac tissues was assessed by Masson staining .The generation of reactive oxygen species (ROS) in the cardiac tissues was detected by dihydroethidium staining .The expression levels of matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinase 2 (TIMP-2) and collagen I in the cardiac tissues were determined by Western blotting.RESULTS:Compared with control group, the cardiac functions were deteriorated in diabetes group (P<0.05), which was improved in treatment group as compared with diabetes group (P<0.05).Com-pared with control group, the formation of collagen and ROS increased significantly in diabetes group (P<0.05), which was decreased in treatment group as compared with diabetes group (P<0.05).Compared with control group, the expres-sion level of MMP-2 in the cardiac tissues was deceased and TIMP-2 was increased significantly in diabetes group (P<0.05), but reversed significantly in treatment group (P<0.05).CONCLUSION: Shenmai injection attenuates cardiac fibrosis in the rats with DCM by inhibiting the generation of ROS .
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