目的 探索水飞蓟素对大鼠肾脏缺血再灌注损伤(IRI)的保护作用及是否与抑制NF-κB活化有关.方法 将30只成年雄性SD大鼠随机为假手术组(S组)、缺血再灌注模型组(IR组)及药物组(SM组).全自动生化分析仪检测血肌酐、血尿素氮,HE染色检测肾小管损伤程度,免疫组织化学检测肾脏IL-6及NF-κB p65表达,酶联免疫吸附法测定肾组织匀浆上清液NF-κB、IL-6浓度.结果 IR组血肌酐、尿素氮、组织匀浆细胞核内NF-κB及细胞浆中IL-6水平较S组升高(P<0.05),SM组较IR组降低(P<0.05),IR组肾小管损伤较重,肾脏IL-6、NF-κB p65表达增强.而给药组肾小管损伤减轻,肾脏IL-6、NF-κB p65表达减弱.结论 水飞蓟素对大鼠肾脏缺血再灌注损伤具有保护作用,其与抑制NF-κB活化有关.%Objective To investigate the protective effect of Silymarin on renal ischemia-reperfusion injury (IRI) and its underlying inhibiting mechanism towards nuclear factor κB (NF-κB). Methods A total of 30 male sprague-dawley (SD) rats were randomly divided into three groups: sham operation (S) group, IRI (IR) group and IRI plus Silymarin (SM) group. Serum creatinine (Cr) and blood urea nitrogen (BUN) were analyzed with automatic biochemical analyzer. Hematoxylin-eosin (HE) staining was performed for histological grading of kidney injury. Expression of interleukin 6 (IL-6) and NF-κB p65 was identified by Immunohistochemical staining and Enzyme-linked immunosorbent assay (ELISA). Results Circulating Cr, BUN, NF-κB and IL-6 were elevated significantly in the IR group compared with those in the S group ( P<0.05), and those in the SM group ( P< 0.05). Animals in the IR group experienced obvious increase of renal tubular damage and expression of IL-6 and NF-κB, which were ameliorated with treatment of Silymarin. Conclusions Inactivation of NF-κB signaling pathway mediates protective effect of Silymarin on renal ischemia-reperfusion.
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