地塞米松对人牙周膜细胞白细胞介素6和白细胞介素8表达的调节作用

Effect of Dexamethasone on the Expression of Interleukin-6 and Interleukin-8 in Human Periodontal Ligament Cells

目的探讨地塞米松(Dex)对人牙周膜细胞(hPDLCs)中白细胞介素(IL)6和IL-8表达的调节作用。方法 Dex或牙龈卟啉单胞菌(P.g)-脂多糖(LPS)分6组处理hPDLCs:10-9mol/L Dex组,10^(-6)mol/L Dex组,10μg/mL P.g-LPS组,10-9mol/L Dex+10μg/mL P.g-LPS组,10^(-6)mol/L Dex+10μg/mL P.g-LPS组,0.1%无水乙醇(对照组)。分别用ELISA法和实时定量PCR法检测IL^(-6)、IL-8蛋白和mRNA表达水平。结果 24 h和48 h时,10-9mol/L Dex组和10^(-6)mol/L Dex组IL^(-6)和IL-8蛋白表达水平显著低于对照组(P<0.05)。48 h时10-9mol/L Dex组和10^(-6)mol/L Dex组hPDLCs IL^(-6) mRNA水平显著低于对照组(P<0.05);而10^(-6)mol/L Dex组IL-8 mRNA的表达水平显著高于对照组(P<0.05)。24 h和48 h时10-9mol/L Dex+10μg/mL P.g-LPS组和10^(-6)mol/L Dex+10μg/mL P.g-LPS组IL^(-6)蛋白和mRNA表达水平显著低于10μg/mL P.g-LPS组(P<0.05)。24 h时10-9mol/L Dex+10μg/mL P.g-LPS组和10^(-6)mol/L Dex+10μg/mL P.g-LPS组IL-8蛋白表达水平显著低于10μg/mL P.g-LPS组(P<0.05),但48 h未见统计学差异。48 h时,10^(-6)mol/L Dex+10μg/mL P.g-LPS组IL-8 mRNA水平显著高于10μg/mL P.g-LPS组(P<0.05)。结论 Dex可以显著抑制hPDLCs固有的和P.g-LPS诱导产生的IL^(-6)的表达,但是Dex对hPDLCs IL-8的表达具有复杂的调节作用,需注意高浓度Dex长时间作用时对hPDLCs IL-8表达的促进作用。

Objective To explore the effect of dexamethasone （Dex） treatment on the expression of interleukin （IL）-6 and IL-8 in human peri- odontal ligament cells （hPDLCs）. Methods hPDLCs were subjected to one of the following treatments for 24 h or 48 h： 109 mol/L Dex; 10-6mol/L Dex; 10 μg/mL Porphyromonas gingivalis （P. g） -lipopolysaceharide （ LPS ） ; 10-9 mol/L Den ＋ 10 μg/mL P. g-LPS ; 10-6 mol/L Dex ＋ 10 μg/mL P. g-LPS; or 0.1% absolute ethyl alcohol （control）. Protein and mRNA expression was detected using ELISA and real-time PCR, respectively. Results At 24 h and at 48 h, IL-6 and IL-8 protein expression in the 109 mol/L I）ex- and 10-6 mo]]L Dex-treated groups was significantly lower than that in the control group （P 〈 0.05）. At 48 h, IL-6 mRNA expression in the 10-9 μ mol/L Dex- and 10-6 mol/L Dex-treated groups was signifi- cantly lower than that in the control group （P 〈 0.05 ）, while IL-8 mRNA expression in the 10-6 mol/L Dex-treated group was significantly higher than that in the control group （P 〈 0.05）. At 24 h and at 48 h,IL-6 protein and mRNA expression in the 10-9 mol/L Dex ＋ 10 μg/mL P. g-LPS- treated group and the 10-6 mol/L Dex ＋ 10 p.g/mL P. g-LPS-treated group was significantly lower than that in the 10 μg/mL P. g-LPS-treated group （P〈 0.05）. At 24 h,IL-8 protein expression in the 10-9 mol/L Dex ＋ 10 p,g/mL P. g-LPS-treated group and the 104 mol/L Dex ＋ 10 μg/mL P. g- LPS-treated group was significantly lower than that in the 10 μg/mL P. g-LPS-treated group （P 〈 0.05）, while no such significant difference exist- ed at 48 h. At 48 h, IL-8 mRNA expression in the 10-6 mol/L Dex ＋ 10 μg/mL P. g-LPS-treated group was significantly higher than that in the 10 μg/mL P. g-LPS-treated group （P 〈 0.05 ）. Conclusion Dex inhibits the innate and P. g-LPS-induced expression of IL-6 in hPDLCs. However, Dex exerts profound effects on IL-8 expression, and treatment with high doses of Dex may promote IL-8 expression over an extended period.