FcγRIIB缺失加重顺铂诱导小鼠的急性肾损伤  

FcγRIIB Deficiency Aggravates Cisplatin-induced Acute Kidney Injury in Mice

作　　者：金筱茜 吴通前 马岚 钟沁 周玲 高健 袁锐 余芳[3,4] N Xiaoqian;WU Tongqian;MA Lan;ZHONG Qin;ZHOU Ling;GAO Jian;YUAN Rui;YU Fang(Department of Clinical Microbiology and Immunology,Guizhou Medcial University,Guiyang 550004,Guizhou,China;Clinical Research Center,Affiliated Hospital of Guizhou Medical University,Guiyang 550004,Guizhou,China;Clinical Laboratory Center,Affiliated Hospital of Guizhou Medical University,Guiyang 550004,Guizhou,China)

机构地区：[1]贵州医科大学临床微生物及免疫学教研室,贵州贵阳550004 [2]贵州医科大学 [3]贵州医科大学附院临床研究中心,贵州贵阳550004 [4]贵州医科大学附院临床检验中心,贵州贵阳550004

出　　处：《贵州医科大学学报》2019年第2期136-140,共5页Journal of Guizhou Medical University

基　　金：国家自然科学基金资助项目(81560266)

摘　　要：目的:探究IgG Fc受体IIB(FcγRIIB)对顺铂诱导小鼠急性肾损伤(AKI)的影响。方法:8～10周龄雄性野生型(FcγRIIB^(+/+)) C57BL/6小鼠、FcγRIIB基因缺失(FcγRIIB^(-/-))小鼠随机分成FcγRIIB^(+/+)对照组、FcγRIIB^(+/+)AKI模型组、FcγRIIB^(-/-)对照组及FcγRIIB^(-/-)AKI模型组,模型组按20 mg/kg体质量腹腔注射顺铂,对照组予同等量生理盐水;注射72 h后,取动脉血检测血清尿素氮(BUN)和血清肌酐(Scr)水平; ELISA检测肾组织匀浆因子TNF-α,IL-6,IL-10水平,HE染色观察肾组织学变化。结果:与FcγRIIB^(+/+)对照组及FcγRIIB^(-/-)对照组比较,FcγRIIB^(+/+)AKI模型组及FcγRIIB^(-/-)AKI模型组BUN和Scr含量升高(P <0. 01)、肾组织匀浆TNF-α及IL-6水平升高(P <0. 01),在FcγRIIB^(-/-)AKI模型组这些改变更为明显,差异有统计学意义(P <0. 01); FcγRIIB^(-/-)AKI模型组肾组织匀浆IL-10水平低于FcγRIIB^(-/-)对照组,差异有统计学意义(P <0. 01); FcγRIIB^(-/-)AKI模型组小鼠较FcγRIIB^(+/+)AKI模型组小鼠肾小管坏死症状严重,其肾小管坏死评分更高(P <0. 01)。结论:缺乏FcγRIIB可加重顺铂诱导AKI。Objective:To explore the effect of FcγRIIB on cisplatin-induced acute kidney injury in a mouse model.Methods:The 8~10 week old male wide type(WT)C57BL/6 and FcγRIIB knock out(FcγRIIB^-/-)mice were randomly divided into FcγRIIB^+/+control group,FcγRIIB^+/+AKI model group,FcγRIIB^-/-control group and FcγRIIB^-/-AKImodel group.Mice in model groups were intraperitoneally administrated with 20 mg/Kg cisplatin for the acute kidney injury(AKI)mouse model induction and the control mice received identical volume of saline instead.After 72 h of injection,the serum levels of urea nitrogen(BUN)and creatinine(Scr)were measured in arterial blood,the levels of TNF-α,IL-6 and IL-10 in renal homogenate were detected by ELISA,and the renal histological changes were observed by HE staining.Results:Compared with FcγRIIB^+/+control group and FcγRIIB^-/-control group,the serum BUN,Scr levels and renal homogenate TNF-α,IL-6 levels increased in FcγRIIB^+/+AKI model group and FcγRIIB^-/-AKI model group(P<0.01),and the changes in FcγRIIB-/-AKI model were more obvious(P<0.01).Renal homogenate IL-10 levels in FcγRIIB^-/-AKI model group were lower than those in FcγRIIB^-/-control group(P<0.01).Mice in FcγRIIB^-/-AKI model group had more severe tubular necrosis symptoms and higher tubular necrosis score than those in FcγRIIB^+/+AKI model group(P<0.01).Conclusion:FcγRIIB deficiency aggravates cisplatin-induced acute kidney injury in mice.

关 键 词：免疫球蛋白Fc受体 顺铂 急性肾损伤 肿瘤坏死因子-α 白细胞介素6 白细胞介素10 

分 类 号：R392.32[医药卫生—免疫学]