口腔医学研究 ›› 2016, Vol. 32 ›› Issue (2): 143-146.DOI: 10.13701/j.cnki.kqyxyj.2016.02.009

• ·临床研究论著· • 上一篇    下一篇

牙龈卟啉单胞菌对人滋养层细胞增殖及凋亡的影响

李磊涛 任洪芋 李宇红 江汉 杜民权*   

  1. 武汉大学口腔医学院·口腔生物医学工程教育部重点实验室 湖北 武汉 430079
  • 收稿日期:2015-05-18 出版日期:2016-02-28 发布日期:2016-03-10
  • 通讯作者: 杜民权,电话:027-87686227
  • 作者简介:李磊涛(1988~),男,山东人,硕士在读,主要从事口腔预防医学研究。
  • 基金资助:
    国家自然科学基金资助项目(编号:81371145

Effect of Porphyromonas Gingivalis Infection on Human Trophoblast Cells Proliferation and Apoptosis.

LI Lei-tao, REN Hong-yu, LI Yu-hong, JIANG Han, DU Min-quan.   

  1. School and Hospital of Stomatology, Key Lab for Oral Biomedical Engineering of Ministry of Education, Wuhan University, Wuhan 430079, China
  • Received:2015-05-18 Online:2016-02-28 Published:2016-03-10

摘要: 目的:检测牙龈卟啉单胞菌感染对人胎盘滋养层细胞(HTR-8细胞)增殖以及凋亡的影响。方法:用不同感染复数(MOI)的牙龈卟啉单胞菌体标准菌ATCC 33277体外感染HTR-8细胞,未感染牙龈卟啉单胞菌的HTR-8细胞作为空白对照组。感染后,用Cell Counting Kit(cck-8)检测HTR-8细胞增殖情况,用线粒体膜电位凋亡检测试剂(JC-1)检测HTR-8细胞凋亡情况。结果:MOI=10组,感染72 h内,HTR-8细胞增殖未受抑制(P>0.05)。而MOI=100组和MOI=200组,感染24 h开始,HTR-8细胞增殖受到明显抑制(P<0.01)。并且与MOI=100组相比,MOI=200组在感染48 h(P<0.05)和72 h(P<0.01)时,HTR-8细胞增殖明显降低。牙龈卟啉单胞菌感染24 h,MOI=200组HTR-8细胞凋亡率显著高于空白对照组(P<0.01)。感染48 h,MOI=100组HTR-8细胞凋亡率显著高于对照组(P<0.01)。MOI=10组在感染24 h和48 h时细胞凋亡率与空白对照组相比差异无统计学意义。结论:在体外感染模型中,牙龈卟啉单胞菌标准菌ATCC 33277感染可抑制滋养层细胞增殖,且促进其凋亡。提示早产低体重儿与牙龈卟啉单胞菌感染引起滋养层细胞增殖和凋亡失衡有关。

关键词: 牙龈卟啉单胞菌, 人胎盘滋养层细胞, 凋亡, 早产低体重

Abstract: Objective: To observe the effect of Porphyromonas gingivalis ATCC 33277 (P.g ATCC 33277) infection on human trophoblast cell line (HTR-8 cells) proliferation and apoptosis in vitro. Methods: HTR-8 cells were infected with P.g at a multiplicity of infection (MOI). Non-infected HTR-8 cells were used as the control. After Infection, the Cell Counting Kit(cck-8)was employed to assay the proliferation of HTR-8 cells. The apoptosis of HTR-8 cells were detected by mitochondrial membrane potential assay kit with JC-1 apoptosis detection kit. Result: At an MOI of 10, no inhibition on HTR-8 cells proliferation was observed following 24-72 h of P.g infection in contrast to the non-infected control (P>0.05). However, P.g significantly inhibited the proliferation of HTR-8 cells at an MOI of 100 or 200 at 24 h (P<0.01). In addition, cells infected with P.g at an MOI of 200 had a significantly lower lever of proliferation than cells infected with P.g at an MOI of 100 at 48 h (P<0.05) and 72 h (P<0.01). Furthermore, following 24 h of infection, P.g at an MOI of 200 significantly increased the rate of apoptosis in HTR-8 cells (P<0.01). A significant higher apoptosis rate in HTR-8 cells was also observed at an MOI of 100 after 48 h of infection (P<0.01). The rate of apoptosis was comparable between the control cells and the infected cells at an MOI of 10 at 24 h or 48 h (P>0.05). Conclusion: Our results demonstrate in vitro that P.g ATCC 33277 infection is able to suppress the proliferation of HTR-8 cells, and in the meantime, enhance the apoptosis of the cells. These results suggest that P.g-induced proliferation and apoptosis imbalance of trophoblast cells is involved in periodontal infection-associated preterm low birth weight.

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