炎症微环境下重组人釉原蛋白对人牙周膜成纤维细胞炎症因子表达的影响

目的 观察在炎症微环境下,重组人釉原蛋白(rhAm)对体外培养的人牙周膜成纤维细胞(hPDLCs)炎症因子表达的影响。方法 体外培养hPDLCs,采用免疫组织化学染色法鉴定hPDLCs。用10μg/m L牙龈卟啉单胞菌(Porphyromonas gingivalis)脂多糖(LPS)模拟炎症微环境,选取20μg/m L rhAm作用于hPDLCs,运用实时荧光定量PCR和ELISA技术检测炎症因子白介素(IL)-1β、IL-6和IL-8的表达。结果 免疫组织化学染色结果证实,培养细胞为hPDLCs。在所检测的4个时间点(6、12、24、72 h),10μg/m L P.gingivalis...

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Published in上海交通大学学报(医学版) Vol. 36; no. 1; pp. 33 - 37
Main Author 廖蔚文 宋忠臣 束蓉 董家辰
Format Journal Article
LanguageChinese
Published 上海交通大学医学院附属第九人民医院牙周病科口腔医学院上海市口腔医学重点实验室,上海,200011 2016
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ISSN1674-8115
DOI10.3969/j.issn.1674-8115.2016.01.007

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Summary:目的 观察在炎症微环境下,重组人釉原蛋白(rhAm)对体外培养的人牙周膜成纤维细胞(hPDLCs)炎症因子表达的影响。方法 体外培养hPDLCs,采用免疫组织化学染色法鉴定hPDLCs。用10μg/m L牙龈卟啉单胞菌(Porphyromonas gingivalis)脂多糖(LPS)模拟炎症微环境,选取20μg/m L rhAm作用于hPDLCs,运用实时荧光定量PCR和ELISA技术检测炎症因子白介素(IL)-1β、IL-6和IL-8的表达。结果 免疫组织化学染色结果证实,培养细胞为hPDLCs。在所检测的4个时间点(6、12、24、72 h),10μg/m L P.gingivalis LPS均可诱导IL-1β、IL-6和IL-8的表达;加入20μg/mL rhAm后,各因子表达均有所降低。结论 rhAm可以抑制炎症微环境下h PDLCs炎症因子的表达。
Bibliography:periodontal ligament cell; inflammatory microenvironment; recombinant human amelogenin; inflammatory factor
LIAO Wei-wen, SONG Zhong-chen, SHU Rong, DONG Jia-chen (Department of Periodontology, College of Stomatology, Shanghai Key Lab of Stomatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China)
31-1259/R
Objective To investigate the effects of recombinant human amelogenin (rhAm) on expressions of inflammatory factors of human periodontal ligament fibroblasts (hPDLCs) cultured in vitro under inflammatory microenvironment. Methods hPDLGs were cultured in vitro and identified by immunohistochemical staining method. The inflammatory microenvironment was simulated by lipopolysaccharide (LPS) with Porphyrornonaz gingivalis of 10 μg/mL and hPDLCs were treated by rhAm of 20 μg/mL. Expressions of inflammatory factors interleukin-1β (IL-1β), IL-6, and IL-8 were detected by real-time PGR and ELISA. Results Results of immunohistochemical staining confirmed that
ISSN:1674-8115
DOI:10.3969/j.issn.1674-8115.2016.01.007