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IRF3抑制LPS诱导肝星状细胞LX-2的炎症因子的分泌 被引量:1

IRF3 suppress the secretion of inflammatory cytokines in the hepatic stellate cell induced by LPS
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摘要 目的研究干扰素调节因子3(IRF3)对LPS诱导的肝星状细胞中LX-2中炎症因子IL-6及TNF-α分泌的影响。方法利用脂质体将质粒pc DNA3-IRF3瞬时转染到人肝星状细胞LX-2中过量表达IRF3,qRT-PCR和Western blot法检测转染效率,并检测炎症因子IL-6及TNF-α的表达。结果qRT-PCR和Western blot结果显示用2μg/ml的LPS刺激LX-2细胞12 h后,与正常组比较,IRF3的表达量明显降低,而诱导产生的炎症因子TNF-α及IL-6的表达量则明显上升。而pc DNA3转入LX-2细胞12 h后,与pc DNA3空载体对照组比较,pc DNA3转染组中炎症因子IL-6及TNF-α表达量在LX-2细胞中被显著抑制。结论在肝星状细胞中,IRF3能够抑制LPS诱导的肝星状细胞LX-2中炎症因子IL-6及TNF-α的表达。 Objective To investigate the effect of IRF3 on the secretion of inflammatory cytokines IL-6 and TNF-αin hepatic stellate cells induced by LPS. Methods Transient transfection of plasmid pcDNA3-IRF3 into LX-2 of human hepatic stellate cells by liposome was used to detect the transfection efficiency,and the expression of inflammatory factor IL-6 and TNF-α was detected by Western blot and qRT-PCR. Results The results of qRT-PCR and Western blot showed that the expression of TNF-α and IL-6 in LX-2 cells stimulated with 2 μg/ml LPS for 12 h was significantly lower than that in normal control group,while the expression of TNF-α and IL-6 increased significantly. However,after pcDNA3 was transfected into LX-2 cells for 12 h,the expression levels of inflammatory factors IL-6 and TNF-α in pcDNA3 transfected group were significantly inhibited in LX-2 cells compared with the control group. Conclusion IRF3 can inhibit the expression of inflammatory cytokines IL-6 and TNF-α in LX-2 induced by LPS.
作者 刘云洁 程玮 李丽 顾萌 徐涛 Liu Yunjie;Cheng Wei;Li Li(Pharmacy Intravenous Admixture Service,The Third Affiliated Hospital of Anhui Medical University,Hefei Binhu Hospital,Hefei 230061;PLA 92752 Troops Health Team,Hefei 231600;School of Pharmacy,Anhui Medical University,Hefei 230032)
出处 《安徽医科大学学报》 CAS 北大核心 2019年第2期178-182,共5页 Acta Universitatis Medicinalis Anhui
基金 安徽医科大学博士科研资助项目(编号:XJ201536) 国家自然科学基金(编号:81700522) 安徽省自然科学基金面上项目(编号:1808085MH235)
关键词 IRF3 TNF-Α 肝星状细胞 LX-2细胞 炎症因子 IRF3 TNF-α hepatic stellate cells LX-2 cells inflammatory factor
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