【摘要】 目的 :参麦注射液对缺血再灌注小鼠肾小管细胞损伤作用的观察。方法 :采用离体培养的鼠肾小管细胞株 ,复制缺血再灌注损伤模型 ,用MTT法测定细胞增殖活性 ,酶组化法观察细胞膜和线粒体中ATP酶和LDH含量的变化 ,用生化法检测小管细胞内SOD活性和MDA含量 ,结果 :不同浓度的SMI对肾小管细胞有明显的促增殖作用 ,在SMI浓度为 5 0 μg·ml 1时 ,促增殖作用最强 ;SMI能显著提高IR后小管细胞的增殖活性和细胞存活率 ;缺血培养 4小时后 ,MDA含量明显增高 ,ATP酶、LDH含量明显降低 ,SMI降低IR培养的小管细胞MDA含量 ,增强SOD活性 ,ATP酶、LDH含量。结论 :SMI具有促进鼠肾小管细胞增殖和减轻肾小管细胞IR损伤的作用 ,其机制可能与增强SOD的活性、加速OFR的清除 ,增强细胞抗氧化的能力 ,减轻膜的脂质过氧化 ,抑制ATP酶含量的减少 ,进而维持生物膜的结构和功能的完整性有关。更多还原

【Abstract】 Objective: To investigate the effects of shenmai injection (SMI) on ischemia reperfusion (IR) injury. Methods: Ischemia reperfusion injury model was made in cultured human renal tubular cells. The proliferative activity of tubular cells was measured with MTT method, ATPase and LDH were measured by histochemistry methods, SOD and MDA were detected by biochemistry methods. Results: The results showed that SMI has a stimulating activity for normal tubular cells proliferation, the greatest activity reached in SMI concentration of 50μg/ml. SMI can also increase the proliferation of ischemia reperfusion injury tubular cells, the survival rate of ischemia reperfusion injured cells and the activity of SOD, ATPase in IR+SMI group were also higher than that in IR group respectivity. While the content of MDA in IR+SMI group was lower than that in IR group. Conclusion: Experimental data indicated that AMI could accelerate the proliferation of renal tubular cells and relieve the ischemia reperfusion injury, possible mechanisms may involve a increasing clearance of oxygen free radical, relieving peroxidation of cell membrane lipids, protecting ATPase from destruction, and may help to maintain a intact structure and function of renal tubular cells.更多还原