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作 者:孟斐[1]
出 处:《当代医学》2010年第34期134-135,共2页Contemporary Medicine
摘 要:目的本研究拟在细胞水平探讨SHP-2参与免疫调节机制的机理,证实了SHP-2与宫颈癌发生的免疫机制有关。方法 SiHa细胞分别与THP-1细胞、SHP-2封闭肽预处理的THP-1细胞进行共培养;ELISA法检测不同处理因素的THP-1细胞培养上清中IL-6的浓度;MTT法检测不同处理因素THP-1细胞对SiHa细胞杀伤作用。结果 MTT检测结果:THP-1细胞组OD值明显高于封闭肽组,两组间差异有统计学意义(q=4.448,p<0.05)。ELISA法检测IL-6的结果:仅培养THP-1细胞的培养上清中IL-6的浓度明显低于给予封闭肽的THP-1细胞培养上清中IL-6的浓度,两组间差异有统计学意义(t=3.533,P<0.05)。结论抑制THP-1细胞中SHP-2的表达后,THP-1细胞分泌的IL-6明显增多,导致它对SiHa细胞的杀伤作用明显增强。SHP-2在宫颈癌的发生中起着重要作用。Objective We want to demonstrate that SHP-2 inhibits proinflammatory cytokine IL-6 production according to cells,identifying SHP-2 as a negative regulator in cervical cancer,and discussing the immune mechanism of cervical cancer.Methods SiHa cell co-culture with THP-1 cell which secreted IL-6 cytokine. After 24hr of co-culture,the cell proliferation was analyzed by performing MTT. Cell culture supernatants were collected from THP-1 cells,THP-1 cells of SHP-2 blocking peptide. The concentration of IL-6 in culture supernatant was assayed using ELISA kit systems.Results MTT experiment:The blocking peptide group has the remarkable difference with the non-treatment factor group,the difference has statistics significance (q=4.448,p〈0.05). ELISA experiment There was a statistically significant difference in the expression of IL-6 between blocking peptide group and non-treatment factor group (t= 3.533,P〈0.05).Conclusion After inhibition expression of SHP-2 in THP-1 cells,THP-1 cells secreted IL-6 significantly increased,leading to its killing effect on SiHa cells significantly increased. SHP-2 negatively regulated IL-6 signaling pathway,inhibition of IL-6 production,eventually leading to cervical cancer.
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