Objective: To analyze the protective effect of PEP-1-superoxide dismutase (SOD)fusion protein pretreatment on renal ischemia-reperfusion injury in mice, and its possible mechanism.Methods: The PEP-1-SOD fusion protein was purified and the mice models of renal ischemia reperfusion injury were established. The PEP-1-SOD fusion protein was pretreated and then reperfused in reperfusion and normal mice. The renal index and the degree of renal injury were scored in three groups. Serum creatinine (Cr) and blood urea nitrogen (BUN) were measured in the three groups of mice. The levels of SOD and malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and myeloperoxidase (MPO) were measured. TUNEL staining was used to detect the apoptosis of renal tissue. Results: The kidney index of pretreatment group and reperfusion group mice were lower than that of the control group (P=0.521, P=0.001), while the pretreatment group mice kidney index was higher than the reperfusion group (P=0.015), the degree of renal injury in the pretreated group and the reperfusion group was higher than that of the control group (P=0.000, P=0.000), pretreatment group mice kidney injury score was lower than the reperfusion group (P=0.000). The levels of BUN and Cr in the pretreatment group were significantly higher than those in the control group (P=0.009, P=0.004), but lower than those in the reperfusion group (P=0.000, P=0.000). The levels of SOD and MDA in the pretreatment group were significantly higher than those in the control group (P=0.559, P=0.000), and the level of SOD was also higher than that in the reperfusion group (P=0.000), but the level of MDA was lower than that of the reperfusion group (P=0.000). The levels of TNF-α and MPO in the pretreatment group were significantly higher than those in the control group (P=0.001, P=0.125), but lower than those in the reperfusion group (P=0.000, P=0.000). The apoptosis rate of renal tissue in the reperfusion group was significantly higher than that in the pretreatment group and the control group, while the pretreatment group was also higher than the control group.Conclusion: PEP-1-SOD fusion protein pretreatment can significantly reduce the renal damage caused by ischemia-reperfusion in mice, the mechanism may be to reduce the level of oxidative stress and apoptosis in vivo, so as to protect the kidney tissue. |
[1] 付凯,袁逸民,蒋昊,等.虾青素在小鼠肾脏缺血再灌注损伤方面的保护作用[J].东南大学学报:医学版,2015,34(2):222-225.
[2] 吴文峰,宁雪,尧永华.右美托咪定预处理对大鼠肝脏缺血再灌注后急性肾损伤的影响[J].中国医药导报,2014,11(3):17-19.
[3] 孙倩.人参皂苷对小鼠肠缺血再灌注致急性肾损伤保护作用中的分子机制研究[D].武汉:武汉大学,2014.
[4] 张永军,王家宁,唐俊明,等.PEP-1-CAT融合蛋白预处理对在体大鼠心肌缺血/再灌注损伤的保护作用[J].郧阳医学院学报,2010,29(4):303-307.
[5] 张友恩,王家宁,唐俊明,等.PEP-1超氧化物歧化酶融合蛋白对大鼠心肌缺血再灌注细胞凋亡的影响[J].中华老年心脑血管病杂志,2009,11(8):603-605.
[6] 董晓伟,王家宁,唐俊明,等.PEP-1-SOD1融合蛋白预处理对大鼠骨髓间充质干细胞在缺氧无血清条件下的保护作用[J].湖北医药学院学报,2011,30(3):258-262.
[7] 汪健,周发明,陈涛,等.PEP-1超氧化物歧化酶对大鼠脑缺血再灌注后Bcl-2的影响[J].现代生物医学进展,2011,11(13):2423-2426.
[8] 陈涛,贾佳,叶飞,等.PEP-1介导铜锌超氧化物歧化酶对帕金森病小鼠氧化应激损伤的保护作用[J].卒中与神经疾病,2012,19(4):199-201,206.
[9] HUANG G Q,WANG J N,TANG J M,et al.The combined transduction of copper,zinc-superoxide dismutase and catalase mediated by cell-penetrating peptide,PEP-1,to protect myocardium from ischemia-reperfusion injury[J].J Transl Med,2011,9(1):73.
[10] 杨波,谭利国,张蕾,等.PEP-1-SOD1融合蛋白抑制血管紧张素Ⅱ诱导的大鼠心脏成纤维细胞Ⅰ型胶原的合成[J].新乡医学院学报,2013,30(8):613-618.
[11] 董敏,席刚明,张正洪,等.PEP-1-SOD1融合蛋白转导入小鼠海马组织的能力及时间关系[J].第四军医大学学报,2009,30(13):1184-1187.
[12] 孟晓燕,黄向阳,王英,等.还原型谷胱甘肽对顺铂致大鼠急性肾损伤氧化应激的影响[J].中外医学研究,2013,11(30):8-9.
[13] 高友光,林献忠,曾振华,等.虎杖苷对脓毒症急性肾损伤大鼠炎症反应和氧化应激的影响[J].临床麻醉学杂志,2017,33(6):584-587.
[14] 丁冠男,刘缚鲲,田鸣,等.丙泊酚预处理减轻肝脏缺血再灌注后急性肾损伤[J].临床和实验医学杂志,2011,10(12):883-885.
[15] 斯妍娜,鲍红光,韩流,等.右美托咪定预先给药和后处理对大鼠肾缺血再灌注损伤的影响[J].中华麻醉学杂志,2012,32(3):301-303. |
