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microRNA-101a与COX-2在尿酸性肾病模型中的变化 被引量:3

The role of microRNA-101a and cycloxygenase-2 in kidney damage induced by hyperuricemia
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摘要 目的:观察micro RNA-101a(mi R-101a)和环氧化酶-2(COX-2)在尿酸性肾病大鼠模型中的变化情况。方法:将24只雄性SD大鼠随机分成3组,即正常对照组(BC组)、模型组(M组)和塞来昔布组(S组),每组各8只,以含酵母和腺嘌呤的饲料喂养造模,21 d后检测各组大鼠血清中肌酐(Cr)、尿素氮(BUN)、尿酸(UA)的含量,并用实时定量PCR技术检测大鼠肾脏皮质中mi R-101a的表达及Wersten Blot法检测COX-2及caspase-3的表达。结果:M组Cr、BUN、UA较BC组升高(P<0.05),S组Cr、BUN、UA较M组降低(P<0.05);M组mi R-101a的表达较BC组明显降低(P<0.05),S组mi R-101a的表达较M组大鼠升高(P<0.05);M组COX-2及caspase-3的表达较BC组明显升高(P<0.05),S组COX-2及caspase-3的表达较M组明显降低(P<0.05)。结论:mi R-101a表达降低及COX-2表达升高可能参与高尿酸引起的肾脏损害的过程,COX-2特异性抑制剂塞来昔布可减轻其损害。 Objective:To investigate the effects of miR-101a and cycloxygenase-2 (COX-2) on rats model of urate nephropathy. Methods:Twenty four rats models of urate nephropathy through fed with yeast and ad-enine for 21 days were divided into three groups, normal control groups, model groups and celecoxib groups. Se-rum creatinine (Cr), blood urea nitrogen (BUN) and blood uric acid (UA) was tested after feeding with yeast and adenine for 21 days. The real time PCR was preformed to analyze the expression of miR-101a and Western Blot was preformed to analyze the expression of COX-2 and caspase-3 in renal cortex. Results:Cr, BUN and UA of model group were signiifcantly higher than that of normal control groups (P〈0.05). The expression of miR-101a in renal cortex from model groups was lower than that of normal control groups (P〈0.05), while higher than that of celecoxib groups (P〈0.05). The expression of COX2 and caspase-3 in renal cortex from model groups were higher than that of normal control group (P〈0.05), while lower than that of celecoxib groups (P〈0.05). Conclu-sion: Decreasing miR-101a and increasing COX2 may involve in kidney damage induced by hyperuricemia, celecoxib as a speciifc inhibitor protects kidney from this damage.
出处 《温州医学院学报》 CAS 2015年第4期256-259,共4页 Journal of Wenzhou Medical College
关键词 尿酸性肾病 microRNA-101a 环氧化酶-2 塞来昔布 凋亡 大鼠 urate nephropathy microRNA-101a cycloxygenase-2 celecoxib apoptosis rats
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