地塞米松及酪氨酸蛋白激酶抑制剂对胃上皮细胞白介素-8分泌抑制作用的实验研究

目的 :探讨慢性胃肠道炎症机制及其防治 ,本文对肿瘤坏死因子和白细胞介素 (白介素 ) 1β诱导的胃上皮细胞白介素 8分泌作用使用地塞米松及酪氨酸蛋白激酶抑制剂进行了体外实验研究。方法 :胃上皮细胞经体外培养后由肿瘤坏死因子和白介素 1β刺激 ,由酶联免疫法检验其白细胞介素 8的分泌 ,并与地塞米松和蛋白激酶抑制剂组相比较。结果 :地塞米松在 10 -8,10 -7,10 -6,10 -5mol/L可抑制肿瘤坏死因子和白介素 1β诱导的胃上皮细胞白介素 8分泌。酪氨酸蛋白激酶抑制剂金雀异黄素和核比霉素A具有类似效应 ,但蛋白激酶C和A抑制剂却无抑制效应。结论 :本文结果提示细胞介素诱导的胃上皮细胞白细胞介素 8的分泌可能是促进胃部炎症性疾病的原因之一 ,抑制白细胞介素 8的产生可为胃肠道炎症的防治机制提供理论依据

Effects of Dexamethasone and protein tyrosine kinase inhibitor on tumour necrosis factor alpha and interleukin 1 beta induced IL-8 production from gastric epithelial cell

Objective: Detailed study of interleukin (IL)-8 regulation and its signal pathways are important in understanding the local inflammatory process and control inflammation.The way to inhibit IL-8 expression in gastric epithelial cells was studied in order to explore the possibility to control the gastric inflammation.Methods: Gastric epithelial cell line MKN-28 was incubated with different doses of tumour necrosis factor (TNF)-α and IL-1β protein kinase inhibitors.The amount of IL-8 release was determined by ELISA.Cell viability was assessed by routine MTT methods.Results: TNF-α and IL-1β induced time and dose dependent IL-8 production in MKN-28 cells. This effect was dose-dependently abolished by Dexamethasone treatment and protein tyrosine kinase (PTK) inhibitor genistein and herbimycin A.Protein kinase (PK) A and C inhibitors had no effect on IL-8 production induced by TNF-α and IL-1β.Conclusion: These results suggest that the inhibition of signal transduction pathways of IL-8 expression on gastric epithelial cell can reduce the IL-8 expression from epithelial cell and subsequently reduce the gastointestinal inflammation.