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本实验采用缺糖的 DMEM,加用高纯氮气 ,造成体外培养的心肌细胞缺糖缺氧性损伤 ,引起心肌胞浆酶 ( LDH和CK等 )的大量释放 ,模拟缺血再灌流损伤。将脉络宁注射液以 1 0 mg/ml、 2 0 mg/ml和 50 mg/ml的浓度加入培养基中 ,观察其对心肌细胞损伤时的 LDH和 CK的释放的影响。结果显示 ,脉络宁注射液浓度为 2 0 mg/ml和 50 mg/ml时 ,对心肌细胞损伤时的心肌胞浆酶的释放有明显抑制作用。并且 ,在显微镜下的心肌细胞形态学观察 ,也可见到模型组的心肌细胞严重裂解 ,细胞变圆、团缩 ,给药组心肌细胞有部分损伤 ,但比模型组的心肌细胞损伤程度明显减轻。从而认为脉络宁注射液对缺氧缺糖性心肌细胞损伤有明显的保护作用。
In this experiment, the lack of sugar DMEM, plus the use of high-purity nitrogen, resulting in myocardial ischemia and hypoxia injury in vitro, causing a large number of myocardial cytosolic enzymes (LDH and CK, etc.) to release a large number of simulated ischemia reperfusion injury. The Mailuoning injection was added to the culture medium at the concentrations of 10 mg/ml, 20 mg/ml, and 50 mg/ml, and the effects on the release of LDH and CK during myocardial cell injury were observed. The results showed that Mailuoning injection concentration of 20 mg/ml and 50 mg/ml significantly inhibited the release of myocardial cytosolic enzymes during cardiomyocyte injury. In addition, under the microscope, the myocardial cell morphology observation also showed that the myocardial cells in the model group were severely lysed and the cells became round and constricted. The myocardial cells in the administration group were partially damaged, but the degree of myocardial cell damage was significantly less than that in the model group. . Therefore, Mailuoning Injection has a significant protective effect against hypoxia- hypoglycemic cardiomyocyte injury.