金筱茜,吴通前,马岚,钟沁,周玲,高健,袁锐,余芳
JIN Xiaoqian,WU Tongqian,MA Lan,ZHONG Qin,ZHOU Ling,GAO Jian,YUAN Rui,YU Fang

• 1:贵州医科大学临床微生物及免疫学教研室
• 2:贵州医科大学
• 3:贵州医科大学附院临床研究中心
• 4:贵州医科大学附院临床检验中心

摘要(Abstract)：

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) C57 BL/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(KeyWords)： 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
immunoglobulin Fc receptor;cisplatin;acute kidney injury;tumor necrosis factor α;interleukin 6;interleukin 10

Abstract:

Keywords:

基金项目(Foundation): 国家自然科学基金资助项目(81560266)

作者(Author): 金筱茜,吴通前,马岚,钟沁,周玲,高健,袁锐,余芳
JIN Xiaoqian,WU Tongqian,MA Lan,ZHONG Qin,ZHOU Ling,GAO Jian,YUAN Rui,YU Fang

DOI: 10.19367/j.cnki.1000-2707.2019.02.003

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