IL-12、LPS对肾小管上皮细胞中lck/P38信号传递的影响

【目的】探讨IL 12、LPS对肾小管上皮细胞中lck基因表达及活性改变的影响 ,明确lck/P3 8信号传递途径在炎症过程的作用。【方法】用原位杂交、放射自显影分别检测lck基因表达及lck活性 ,用免疫印迹法对肾小管上皮细胞在IL 12、LPS刺激下其P3 8磷酸化进行测定。【结果】肾小管上皮细胞经IL 12 ,LPS刺激后lckmRNA表达水平增高 ,lck活性在刺激后 5min时最强 ,加入lck抑制剂PP1,IL 12刺激lck活性明显减弱。IL 12及LPS可以促进肾小管上皮细胞中P3 8活化、磷酸化 ,在 15min时最强 ,加入lck抑制剂后则抑制IL 12刺激时的P3 8磷酸化 ,而LPS刺激组不明显。【结论】IL 12 ,LPS可通过促进肾小管上皮细胞中lck/P3 8活化 ,参与炎症过程。

Effect of IL-12 and LPS on lck/P_(38) Signalling Pathaways in Tubular Epithelium

Objective In order to investigate IL 12 and LPS on Lck gene expression and its activity in renal tubular epithelial cells(TEC) and clarify roles of IL 12 and P 38 signalling pathways involved in inflammation. Methods mRNA expression of lck and lck activity were determined by in situ hybridization and autoradiography respectively. P 38 phosphorylation upon IL 12 and LPS stimulations was detected by Western blot analysis. Results Increased mRNA expression of lck was observed after stimulation of TEC with IL 12 and LPS .The maximal effect on lck activity was present at 5 min after stimulation and the activity of lck was martly decreased upon IL 12 treatment in the presence of lck selective inhibitor PP1. Moreover, IL 12 and LPS may induce the phosphorylation of P 38 in TEC, maximal phosphorylation occurred at 15 min after stimulation. In addition, PP1 inhibited the phosphorylation of P 38 induced by IL 12. Conclusion IL 12 and LPS are involved in inflammation via the activation of lck/P 38 in TEC.