【摘要】 目的探讨促红细胞生成素(EPO)对糖尿病(DM)鼠造影剂急性肾损伤(CI-AKI)的保护作用及其机制。方法 SD实验大鼠28只,随机分为正常组(CON组,n=7),糖尿病组(DM组,n=7)、造影剂组(CM组,n=7)、EPO预处理组(EPO组,n=7)。观察造影后各时间点6 h、12 h、24 h、48 h、72 h血肌酐(Scr)、尿肾损伤因子(Kim-1)的变化。并检测肾皮质内丙二醛(MDA)含量、超氧化物歧化酶(SOD)的活性变化。结果与DM组相比,CM组第48 h肾皮质MDA含量升高,SOD活性下降,而EPO组肾皮质MDA含量下降,SOD活性升高;CM组Scr第6 h、12 h差异无统计学意义(P>0.05),24 h、48 h、72 h均显著升高(P<0.05),EPO组Scr 24 h、48 h、72 h则显著下降(P<0.01);尿Kim-1各时间点CM组较CON组显著增加(P<0.05),而EPO组较CM组则显著减少(P<0.05)。结论促红细胞生成素预处理能降低急性肾损伤后Scr、Kim-1的水平,抑制氧化应激反应,减轻糖尿病大鼠造影剂所致的急性肾损伤。更多还原

【Abstract】 Objective The objective of the study was to explore the protective effect of hemopoietin(EPO) against contrast medium-induced acute kidney injury(CI-AKI) in rats with diabetes mellitus(DM) and investigate its mechanism. Methods 28 SD rats were randomly divided into a normal group(CON, n=7), a diabetes group(DM, n=7), a contrast medium group(CM, n=7), and an EPO pretreatment group(EPO, n=7). The changes in serum creatinine(Scr) and urine kidney damage factor(Kim-1) levels were observed at 6 h, 12 h, 24 h, 48 h, and 72 h after radiography; and the changes in malondialdehyde(MDA) level in the renal cortex and activity of superoxide dismutase(SOD) were also measured. Results As compared with the DM group, the CM group had an increase in MDA in the renal cortex and a decrease in SOD activity at 48 h, while the EPO group had decreased level of MDA in the renal cortex and an increased activity of SOD. Scr level of the CM group did not vary at 6 h and a 12 h(P>0.05), but significantly increased at 24 h, 48 h, and 72 h(P<0.05); in contrast, Scr level of the EPO group decreased significantly at 24 h, 48 h, and 72 h(P<0.01). At all time points, the CM group had significantly higher urine Kim-1 than the CON group(P<0.05), and the EPO group had significantly lower urine Kim-1 than the CM group(P<0.05). Conclusion Pretreatment with hemopoietin can reduce the levels of Scr and Kim-1 after acute kidney injury, suppress oxidative stress responses, and alleviate contrast medium-induced acute kidney injury in diabetic rats.更多还原