目的观察维甲酸相关孤儿受体(retinoid-related orphan receptor,ROR)γt、白介素(IL)-17在实验性Ig A肾病大鼠中的表达情况,以及骨化三醇对RORγt、IL-17的调节作用。方法 30只雄性Wistar大鼠随机抽取20只,建立Ig A肾病大鼠模型,再随机分为Ig A肾病组(n=10)、骨化三醇治疗组(n=10),另10只为正常对照组。骨化三醇治疗组采用骨化三醇(10 ng/100 g体重)灌胃治疗,其他两组不予治疗。2周后处死大鼠,取肾脏冰盐水冲洗后切块,以逆转录聚合酶链反应(RT-PCR)法检测RORγt mRNA及IL-17 mRNA的表达水平;处死前常规检测3组24 h尿蛋白、尿红细胞计数、血肌酐水平。结果经光镜及免疫荧光检查证实造模成功。Ig A肾病组与正常组比较,24 h尿蛋白含量、尿红细胞计数、RORγt mRNA、IL-17 mRNA的表达水平均显著升高(P均〈0.01);骨化三醇治疗组与Ig A肾病组比较,上述指标均显著降低(P均〈0.01),但仍高于正常对照组(P均〈0.01)。结论RORγt、IL-17可能参与Ig A肾病的发生、发展;骨化三醇可能通过直接或间接下调RORγt、IL-17的表达,对Ig A肾病有一定治疗作用。
objective To observe the expressions of retinoid-related orphan receptor( ROR) γt and interleukin( IL)-17 and the regulating effect of calcitriol on them in rats with Ig A nephropathy. Methods Out of 30 male Wistar rats,20 were randomly selected to set up the model of Ig A nephropathy including Ig A nephropathy group and calcitriol treatment group( n = 10 each),and the remaining 10 rats were served as normal control group. Calcitriol was administered by gavage( 10 ng/100 g body weight) in calcitriol treatment group,and no treatment was given in the other groups. All rats were killed two weeks late. The kidney was taken and cut into pieces after salt water washing to detect the expression levels of RORγt mRNA and IL-17 mRNA by reverse transcription-polymerase chain reaction( RT-PCR). The 24-hour urine protein,urine red blood cell count and serum creatinine were routinely examined before killing the rats. Results Confirmed by light microscope and immunofluorescence examination,the model of Ig A nephropathy was successfully established. The content of24-hour urinary protein,urine red blood cell count and the expression levels of RORγt mRNA and IL-17 mRNA in Ig A nephropathy group increased significantly compared with normal control group( all P〈0. 01). The aforementioned indexes in calcitriol treatment group decreased significantly compared with Ig A nephropathy group( all P〈0. 01) but were still higher than those in normal control group( all P〈0. 01). Conclusions RORγt and IL-17 may participate in the occurrence and development of Ig A nephropathy. Calcitriol may play a therapeutic role for Ig A nephropathy by down-regulating the expressions of RORγt and IL-17 directly or indirectly.