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纸质出版:2012
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王春,向学熔,杨明聪,陈芳淳.青藤碱对牙龈卟啉单胞菌脂多糖诱导的人牙龈成纤维细胞IL-8表达的影响[J].陆军军医大学学报(原第三军医大学学报),2012,34(19):1972-1976.
Wang Chun,Xiang Xuerong,Yang Mingcong,Chen Fangchun.Effect of sinomenine on IL-8 expression in porphyromonas gingivalis lipopolysaccharide-stimulated human gingival fibroblasts[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(19):1972-1976.
王春,向学熔,杨明聪,陈芳淳.青藤碱对牙龈卟啉单胞菌脂多糖诱导的人牙龈成纤维细胞IL-8表达的影响[J].陆军军医大学学报(原第三军医大学学报),2012,34(19):1972-1976. DOI:
Wang Chun,Xiang Xuerong,Yang Mingcong,Chen Fangchun.Effect of sinomenine on IL-8 expression in porphyromonas gingivalis lipopolysaccharide-stimulated human gingival fibroblasts[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(19):1972-1976. DOI:
目的 探讨青藤碱对牙龈卟啉单胞菌脂多糖诱导的人牙龈成纤维细胞表达IL-8的影响。 方法 用不同浓度的青藤碱(25、50、100 μmol/L)预处理24 h后,再加入1 μg/ml的脂多糖(LPS)处理人牙龈成纤维细胞。采用RT-PCR、ELISA法检测青藤碱对脂多糖诱导细胞表达IL-8的影响;用Western blot法检测青藤碱对NF-κB核转位及IκBα降解的影响。加入NF-κB抑制剂Bay11-7085 10 μmol/L、TPCK 20 μmol/L预处理细胞24 h后,再用LPS刺激细胞4 h,采用ELISA法检测NF-κB抑制剂对脂多糖诱导的IL-8表达的影响。 结果 青藤碱剂量依赖性地抑制脂多糖诱导的人牙龈成纤维细胞中IL-8 mRNA及蛋白表达(P0.05);与脂多糖组比较,青藤碱基本上把NF-κB阻滞在细胞质中,而细胞经脂多糖处理1 h后,大部分NF-κB被转运到细胞核中,经100 μmol/L青藤碱预处理细胞的细胞质中NF-κB含量为脂多糖组的2倍;脂多糖处理细胞1 h后,50%的IκBα降解,但经青藤碱预处理细胞后,呈浓度依赖性抑制脂多糖诱导IκBα的降解(P0.05)。50 μmol/L的青藤碱使脂多糖诱导IκBα的降解恢复到正常水平;脂多糖处理组IL-8表达量为对照组的2.4倍,但加入NF-κB抑制剂Bay11-7085(10 μmol/L)、TPCK(20 μmol/L)后IL-8蛋白的表达量分别下降为对照组的1.8倍和1.6倍。 结论 青滕碱可能通过阻断NF-κB的核转位以及IκBα的降解来抑制牙龈卟啉单胞菌脂多糖诱导的人牙龈成纤维细胞IL-8的合成。
Objective To study the effect of sinomenine (Sin) on IL-8 expression in porphyromonas gingivalis lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (HGF). Methods HGF were pretreated with Sin at the concentrations of 25
50 and 100 μmol/L for 24 h and then with 1 μg/ml LPS which was added into Sin. Effect of Sin on LPS-mediated IL-8 expression in HGF was detected by RT-PCR and ELISA
respectively. Effect of Sin on NF-κB translocation and IκB degradation was detected by Western blotting. Effect of NF-κB inhibitors
Bay11-7085 (10 μmol/L) and TPCK (20 μmol/L)
on Sin-mediated IL-8 expression in HGF
was detected by ELISA 24 h after pretreatment followed by 4 h-LPS stimulation. Results Sin suppressed the IL-8 mRNA and protein expressions in LPS-mediated HGF in dose-dependent manner (P0.05). SIN could almost keep the NF-κB in the cytoplasm compared with LPS. Most NF-κB was transported in the nuclei 1 h after LPS treatment. The NF-κB level was 2-fold higher than the LPS level in cytoplasm after Sin (100 μmol/L) pretreatment. Fifty percent of IκBα was degraded 1 h after the HGF were pretreated with LPS and Sin inhibited the LPS-mediated degradation of IκBα in a dose-dependent manner after HGF were pretreated (P0.05). Sin (50 μmol/L) pretreatment returned the LPS-mediated IκBα degradation to its normal levels. The IL-8 expression level was 2.4-fold higher in LPS pretreatment group than in control group
and 1.8-fold and 1.6-fold lower in LPS pretreatment group than in control group after pretreatment with NF-κB inhibitors
Bay11-7085 (10 μmol/L) and TPCK (20 μmol/L). Conclusion Sin inhibits the porphyromonas gingivalis LPS-mediated IL-8 expression in HGF by blocking the NF-κB translocation and the IκBα degradation.
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