JIANG Gui xing *, CUI Yun fu, CAO Li ping, et al. Effects of interleukin 6 in wound healing of human biliary epithelial cells[J]. Chinese Journal of Digestive Surgery, 2012, 11(5): 471-475. DOI: 10.3760/cma.j.issn.1673 9752.2012.05.019
Citation: JIANG Gui xing *, CUI Yun fu, CAO Li ping, et al. Effects of interleukin 6 in wound healing of human biliary epithelial cells[J]. Chinese Journal of Digestive Surgery, 2012, 11(5): 471-475. DOI: 10.3760/cma.j.issn.1673 9752.2012.05.019

Effects of interleukin 6 in wound healing of human biliary epithelial cells

  • Objective To investigate the mechanism of interlekin 6 (IL 6) in wound healing of human biliary epithelial cells (BECs). Methods BECs were cultured in IL 6 at different concentrations: 0 ng/L (0 ng/L group), 10 ng/L (10 ng/L group), 50 ng/L (50 ng/L group), 100 ng/L (100 ng/L group), 1000 ng/L (1000 ng/L group). The effects of IL 6 on the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and the expression of trefoil family factors 3 (TFF3) were detected. BECs were divided into untreated group, STAT3 RNAi group (BECs transfected with STAT3 RNAi adenovirus) and Control RNAi group (BECs transfected with vacant RNAi adenovirus). The effects of IL 6 on the expression of TFF3 were detected after RNAi of STAT3. In vitro wound models were constructed for the untreated group, STAT3 RNAi group and Control RNAi group, and the effects of IL 6 and TFF3 on BECs of the 3 groups were detected. All data were analyzed by using the Student′s t test, analysis of variance or Sidak test. Results The expressions of phosphorylated STAT3 in the 50 ng/L group, 100 ng/L group and 1000 ng/L group were 0.240±0.052, 0.714±0.124, 0.327±0.069, respectively, which were significantly higher than 0.033±0.011 of the 0 ng/L group (q=5.246, 17.260, 7.451, P<0.05). The contents of mRNA and protein of TFF3 increased as the increase of IL 6 concentration (q=12.045, 9.889, P<0.05). After RNAi of STAT3 of the BECs, the expression of TFF3 decreased when the concentration of IL 6 was 1000 ng/L. The expression of TFF3 of the STAT3 RNAi group was 0.037±0.005, which was significantly lower than 0.267±0.038 of the Control RNAi group and 0.301±0.042 in the untreated group (q=12.135, 13.929, P<0.05). In the in vitro wound model, the speed of BECs migration in the STAT3RNAi group was (9.1±1.5)μm/h, which was slower than (25.1±3.8)μm/h of the Control RNAi group after 12 hours of interference with IL 6 (q=7.737, P<0.05). The speed of BECs migration of STAT3 RNAi group was (39.2±4.7)μm/h after adding 1 g/L of recombinant TFF, which was significantly faster than that of the Control RNAi group (q=14.507, P<0.05). Conclusion IL 6 promotes cell migration and wound healing by activating STAT3 and up regulating TFF3 expression.

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