AIM : To investigate the effect of advanced glycation end products ( AGEs) on proliferation and osteogenic differentiation of lipopolysaccharide ( LPS)-stimulated human periodontal ligament stem cells ( HPDLSCs).METHODS : The effects of LPS and AGEs on the proliferation of HPDLSCs were analyzed by MTT assay.The expressions of interleukin-6 ( IL-6 ) , alkaline phosphatase ( ALP) and Runt-related transcription factor-2 ( RUNX-2) mRNA of HPDLSCs which were stimulated by LPS ( 1O μg/mL) and AGEs (100 μg/mL) were detected by RT-PCR.RESULTS : MIT assay showed that LPS and AGEs inhibited the proliferation of HPDLSCs in a dose dependent manner.LPS stimulation significantly increased IL - 6 expression and inhibited ALP and RUNX-2 expression in HPDLSCs.Co -stimulation of HPDLSCs with LPS and ACEs markedly enhanced the effects of LPS on IL-6, ALP and RUNX -2 expression.CONCLUSION : LPS and ACEs inhibited the proliferation of HPDLSCs in a concentration-dependent manner.AGEs can enhance the stimulatory effects of LPS in up - regulating IL-6 expression and the inhibitory effects of LPS in down-regulating osteogenic factors expression.Our results suggest that diabetes may increase the degree of periodontal inflammation in patients with periodontitis.%目的:探讨糖基化终末产物(AGEs)对脂多糖(LPS)介导下的人牙周膜干细胞(HPDLSCs)增殖和骨向分化能力的影响.方法:HPDLSCs培养和鉴定;MTT法检测不同浓度LPS和AGEs对HPDLSCs增殖能力的影响;Real Time-PCR检测10μg/mL LPS和100μg/mL LAGE<,s>刺激HPDLSCs后白细胞介素-6(IL-6)、碱性磷酸酶(ALP)和Runt-related transcription factor2(RUNX-2)mRNA的表达水平.结果:与正常组比较,10、100μg/mL LPS均抑制HPDLSCs的增殖,50、100、200 μg/mL AGEs均抑制HPDLSCs的增殖,100、200 μg/mL AGEs比50μg/mL AGEs抑制明显,差异有统计学意义(P<0.05);在成骨诱导下10μg/mL LPS刺激HPDLSCs 6 d和10μg/mL LPS刺激HPDLSCs 3 d后再加10 μg/mL LPS/100μg/mL AGES共同刺激3 d,后者较前者IL-6表达明显增加,ALP和RUNX-2的表达降低,差异有统计学意义(P<0.05).结论:LPS和AGEs均成浓度依赖性抑制HPDLSCs的增殖能力.AGEs能使LPS介导下的HPDLSCs的炎性因子表达增强,成骨分化能力降低.提示糖尿病可能会加重牙周炎病人的牙周炎炎症程度.
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