白细胞介素-12信号转导参与小鼠肾小管上皮细胞炎性损伤

IL-12 signaling pathway in murine renal tubular epithelial inflammatory injury

为观察白细胞介素 12 (IL 12 )在小鼠肾小管上皮细胞 (TEC)炎症损伤的信号传递 ,以培养的正常小鼠TEC作为空白对照组 ,狼疮肾炎 (LN)TEC作为实验组 ,以IL 12 (10 μg/L)刺激 5min ,利用放射自显影检测发现正常对照及LN组lck活性增强 ,后者更明显 ,应用lck抑制剂PP1后其活性消失。再以等浓度IL 12刺激TEC 15min ,采用免疫印迹法观察到LN组P38磷酸化强于正常对照组 ,应用PP1或P38抑制剂SB2 0 35 80则不发生P38磷酸化。给予IL 12刺激时发现LN组c Jun基因表达水平强于正常对照组 ,应用PP1或SB2 0 35 80后则未有c Jun基因表达 ,提示IL 12可通过lck/P38/c

In order to investigate IL 12 signaling pathway in murine renal tubular epithelial injury, the mice were divided into following two groups in the experiment: normal mouse group and lupus nephritis (LN) group Lck activity detected by autoradiograph were enhanced after treatment of tubular epithelium (TEC) from both groups with IL 12 (10μg/L) The lck activity of TEC from LN group was higher than that from normal group, the maximal effects was noted 5min after stimulation, the activity was diminished in the presence of lck inhibitor PP 1 P 38 phosphorylation of TEC from LN groups was stronger than that from normal group determined with immune blot The phosphorylation of P 38 occurred 15min after IL 12 treatment of TEC PP 1 and P 38 specific inhibitor SB203580 blocked IL 12 induced P 38 phosphorylation There was increased expression of c Jun of IL 12 stimulated TEC from the LN group compared to that observed in similarly treated T cells from normal group, while c Jun expression wasn't detected in the presence of PP 1 and SB203580: These results indicated that IL 12 exert biologic effect in TEC through lck/P 38 /c Jun signaling pathways, IL 12 was involved in inflammatory injury vial its aberrant biologic role