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目的观察狼疮肾炎病理过程中淋巴细胞特异性蛋白酪氨酸激酶(Lck)在肾小管上皮细胞内的表达及白细胞介素-2(IL-2)对其表达的影响。方法体外培养6周龄BXSB狼疮小鼠的近端肾小管上皮细胞,给予IL-2刺激,采用反转录聚合酶链反应(RT-PCR)方法及免疫印迹法检测肾小管上皮细胞中Lck mRNA和蛋白的表达,观察IL-2对Lck表达水平的影响。同时用免疫组织化学方法观察Lck蛋白在狼疮肾炎小鼠和人类肾脏组织标本肾小管上皮细胞内的表达情况。结果体外培养的6周龄BXSB狼疮小鼠近端肾小管上皮细胞中仅有微量LckmRNA及蛋白的表达,IL-2刺激后表达水平显著增加(P<0.05)。免疫组织化学方法显示:正常BALB/C小鼠、未发病的狼疮小鼠和人类微小病变性肾病肾脏组织的肾小管上皮细胞内均未发现明显的Lck蛋白表达,而已发病的16周龄狼疮肾炎小鼠和人类Ⅳ型狼疮肾炎肾脏组织标本的肾小管上皮细胞内则有明显的Lck蛋白表达。结论IL-2可活化肾小管上皮细胞并诱导Lck表达,Lck可能作为细胞因子或炎症因子的重要信号分子,在小管-间质性炎症及狼疮肾炎病理过程中发挥着重要作用。
Objective To observe the expression of lymphocyte-specific protein tyrosine kinase (Lck) in renal tubular epithelial cells and the effect of interleukin-2 (IL-2) on the expression of Lck nephritis. Methods The proximal tubular epithelial cells of 6-week-old BXSB lupus mice were cultured in vitro and stimulated with IL-2. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to detect the expression of Lck mRNA in renal tubular epithelial cells And protein expression, the impact of IL-2 on Lck expression levels. Immunohistochemistry was used to observe the expression of Lck protein in renal tubular epithelial cells of lupus nephritis and human kidney tissues. Results The expression of LckmRNA and protein in proximal tubular epithelial cells of 6-week-old BXSB lupus mice cultured in vitro was significantly increased (P <0.05) after IL-2 stimulation. Immunohistochemistry showed that no significant expression of Lck protein was found in normal BALB / C mice, uninflammatory lupus mice and renal tubular epithelial cells in human minimal lesion nephropathy, whereas the incidence of 16-week-old lupus nephritis Lack protein expression was observed in renal tubular epithelial cells of mouse and human type IV lupus nephritis kidney specimens. Conclusion IL-2 can activate renal tubular epithelial cells and induce Lck expression. Lck may be an important signaling molecule of cytokines or inflammatory cytokines and play an important role in the pathological process of tubulointerstitial inflammation and lupus nephritis.