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作 者:倪茗[1]
机构地区:[1]武汉科技大学附属汉阳医院妇产科,湖北武汉430050
出 处:《海南医学院学报》2015年第8期1023-1026,共4页Journal of Hainan Medical University
基 金:湖北省卫生厅医学科研基金课题(JX2B51)~~
摘 要:目的:探讨脂多糖(LPS)体外诱导的子宫内膜炎对核因子-κB(NF-κB)信号通路的炎症蛋白和氧化因子的影响。方法:用不同浓度LPS(50、100、200ng/mL)对子宫内膜细胞进行诱导,MTT法检测细胞活力,ELISA试剂盒检测细胞上清白介素-1(IL-1)及前列腺素E2(PGE2)浓度,硫代巴比妥酸法检测丙二醛(MDA)含量,Gries法检测一氧化氮(NO)含量,黄嘌呤氧化法检测超氧化物歧化酶(SOD)活性,western blot检测NF-κB p65的表达及磷酸化情况。结果:随着LPS诱导剂浓度的增加,子宫内膜细胞活力下降,且在48h达到最大抑制程度,细胞上清中SOD活性下降,MDA、NO、IL-1及PGE2含量显著上升,NF-κB p65磷酸化显著。结论:LPS能诱导子宫内膜细胞产生炎症,刺激细胞炎症因子的分泌和抗氧化能力的降低,与NF-κB信号通路有关。Objective: To explored effect of endometritis induced by LPS on level of inflammatory protein and oxidation factor via NF-KB signaling pathway. Methods.. Endometial cell was treated with LPS (50, 100, 200 ng/mL). The viability of cell was detected by MTT assay. The concentration of IL-6 and PGE2 was tested by elisa method. The concentration of MDA was tested by thiobarbituric acid method. The concentration of SOD was tested by xanthine oxidation method. The concentra- tion of NO was tested by gries method. The expression of NF-KB p65 was assayed by western blot. Results; MTT assay dem- onstrated LPS (50, 100, 00 ng/mL) could suppressed cell viability, and the inhibitory effect was highest in 48 h. With the in- creasing dose of LPS, the activity of SOD decreased, the level of MDA, NO, IL-1 and PGE2 elevated. Finally, LPS stimula- ted NF-KB p65 phosphorylation. Conclusions: These results suggests that endometrial cell treated by LPS can induce inflamma- tiory factor secreted and anti-oxidant ability decreased, which might be related to NF-xB signal pathway.
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