LPS对肝癌细胞TLR4及IL-23/IL17A表达的影响  被引量:3

Effect of LPS on the expression of TLR4,IL-23 and IL-17A in HepG2 cell line

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作  者:康玉明[1] 苏国爱 张艳丽[3] 

机构地区:[1]宁夏医科大学总医院肝胆外科,宁夏银川750004 [2]北京仁和医院,北京102600 [3]宁夏医科大学基础医学院,宁夏银川750004

出  处:《宁夏医学杂志》2017年第1期6-8,共3页Ningxia Medical Journal

基  金:宁夏自然科学基金资助项目(NZ14139)

摘  要:目的观察Toll样受体4(TLR4)的激动剂LPS(LPS)对肝癌HepG2细胞株表达TLR4、IL-23/IL-17A的影响,探讨TLR4、IL-23/IL-17A在肝癌发生中的作用及可能机制。方法用LPS 1 mol/L作用HepG2细胞24 h,或先用LPS作用HepG2细胞24 h后再用髓样分化因子-88(My D88)的阻断剂ST2825作用HepG2细胞8h,运用Q-PCR法检测TLR4、IL-23、IL-17A在HepG2细胞的转录水平;应用Western-blot方法测定TLR4、IL-23及IL-17A在HepG2细胞的表达,采用ELISA法检测HepG2细胞培养上清液中IL-23在12 h、24 h、36 h的分泌水平。结果 LPS可促进HepG2细胞株IL-23的分泌和TLR4、IL-23、IL-17A m RNA的转录及蛋白表达,阻断My D88后其表达水平比LPS组明显降低,趋于正常组水平。结论 TLR4、IL-23及IL-17A参与原发性肝癌的发生与进展。Objective To explore the effect of TLR4 agonist lipopolysaccharides( LPS) on the expression of interleukin- 23( IL-23) and IL-17 A in HepG2 cell line,to analyze the mechanism of TLR4,IL-23 and IL-17 A in carcinogenesis of hepatocellular carcinoma. Methods HepG2 cells were stimulated with LPS 24 h,then treated HepG2 cells 8h with Myeloid differentiation factor 88( My D88)and inhibitors ST2825. The m RNA level of TLR4,IL- 23 and IL- 17 A in HepG2 cells was detected by Q- PCR. The expression of TLR4,IL- 23 and IL- 17 A was measured by Western- blot; The level of IL- 23 was measured by ELISA at 12 h,24 h and 36 h. Results LPS promoted m RNA transcription level of TLR4,IL- 23 and IL- 17 A in HepG2 cell lines and the protein expression of TLR4,IL- 23,IL-17 A,while ST2825 inhibited the expression of TLR4,IL- 23,IL- 17 A. LPS enhanced the secreted level of IL- 23 in different time-phase. Conclusion TLR4,IL- 23 and IL- 17 A are involved in the occurrence and progress of hepatocellular carcinoma.

关 键 词:肝癌 Toll样受体 白介素-23 白介素质-17A 

分 类 号:R735.7[医药卫生—肿瘤]

 

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