摘要
目的:统计PEP-1-SOD融合蛋白预处理对小鼠缺血再灌注肾损伤的保护效果,分析其可能的作用机制。方法:纯化PEP-1-SOD融合蛋白,建立缺血再灌注肾损伤小鼠模型,然后先给予预处理组小鼠PEP-1-SOD融合蛋白然后再灌注,并以再灌注及正常小鼠作为对照。统计3组小鼠的肾脏指数及肾损伤程度评分,检测3组小鼠血清中血清肌酐(Cr)和尿素氮(BUN)含量,检测小鼠肾组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因-α(TNF-α)、髓过氧化物酶(MPO)的水平,并采用TUNEL染色方法对肾组织细胞凋亡进行检测。结果:预处理组及再灌注组小鼠肾脏指数均低于对照组(P=0.521,P=0.001),而预处理组小鼠肾脏指数高于再灌注组(P=0.015)。预处理组及再灌注组小鼠肾损伤程度评分均高于对照组(P=0.000,P=0.000),预处理组小鼠肾损伤程度评分低于再灌注组(P=0.000)。预处理组小鼠BUN、Cr均高于对照组(P=0.009,P=0.004),而均低于再灌注组(P=0.000,P=0.000),SOD、MDA水平均高于对照组(P=0.559,P=0.000),SOD水平也高于再灌注组(P=0.000),但MDA水平却低于再灌注组(P=0.000),TNF-α、MPO水平均高于对照组(P=0.001,P=0.125),却均低于再灌注组(P=0.000,P=0.000)。再灌注组小鼠肾脏组织细胞凋亡率明显高于预处理组及对照组,而预处理组小鼠也高于对照组。结论:PEP-1-SOD融合蛋白预处理可以明显降低小鼠缺血再灌注造成的肾损伤,作用机制可能为降低体内氧化应激水平和细胞凋亡,从而保护肾脏组织。
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.
作者
曾艳
张任
赵韶静
ZENG Yan, ZHANG Ren, ZHAO Shao-jing(Department of Nephrology, Oongfeng Hospital Affiliated to Hubei University of Medicine, Shiyan 442008, Chin)
出处
《现代医学》
2018年第3期239-243,共5页
Modern Medical Journal
基金
湖北省教育厅科学研究计划指导性项目(B2015488)