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炎性骨组织中miR-23a和miR-30a的表达改变及其生物学作用的研究 被引量:5

miR-23a and miR-30a expression in inflammatory bone tissues and cells
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摘要 目的:观察研究体外炎性微环境下的牙周膜细胞(periodontal ligament cells,PDLCs)、成骨细胞(MC3T3-E1)和体内大鼠牙周炎牙龈组织、骨组织中miR-23a和miR-30a的表达变化,证实miR-23a和miR-30a在牙周炎性骨缺失中发挥重要调控作用,探讨其生物学作用。方法:1μg/mL LPS刺激PDLCs、MC3T3-E1细胞模拟炎性微环境,24 h后收集细胞。采用正畸结扎丝结扎各SD大鼠右侧上颌第一磨牙颈部,左侧未结扎作为自身对照,21 d后取其牙龈、牙槽骨组织。采用荧光定量PCR分别检测处于炎性微环境下的细胞、大鼠牙周炎牙龈组织、牙周骨组织中miR-23a和miR-30a的表达。结果:炎性环境下PDLCs、MC3T3-E1细胞中miR-23a和miR-30a的表达水平均较对照组明显增高(P<0.05)。大鼠牙周炎牙龈组织、牙槽骨组织中miR-23a和miR-30a的表达水平明显高于正常对照侧(P<0.05)。结论:miR-23a和miR-30a参与调控炎性环境下骨代谢和成骨细胞活性。 AIM: To observe the expressions of miR-23a and miR-30a in periodontal ligament cells (PDLCs) and osteoblast MC3T3-El cells, and in the gingiva and alveolar bone tissues of rats with periodontitis. METHODS :The PDLCs and MC3T3-E1 cells were stimulated with 1 p,g/mL LPS for 24 h to imitate inflammatory en- viorenment. 5 SD rats were received wire ligatures aroud the cervix of the right first maxillary molar while the contralat- eral tooth was untreated as the control. Gingiva and alveolar bone tissues were collected after 21 days. RT-PCR was used to examine the expressions of miR-23a and miR-30a in the cells and tissues. RESULTS:After 24 h induction the expression of miR-23a and miR-30a in LPS-stimulated cells was significantly higher than in the controls ( P 〈 0.05 ). The expression of miR-23a and miR-30a in inflammatory gingiva and alveolar bone tissues was significantly higher than in the healthy tissues ( P 〈 0.05 ). CONCLUSION: miR-23 a and miR-30a may regulate the metabolism of bone tissue and the biological characters of osteoblasts and PDLCs in inflammatory micro-envioronment.
出处 《牙体牙髓牙周病学杂志》 CAS 北大核心 2013年第4期231-234,共4页 Chinese Journal of Conservative Dentistry
基金 国家自然科学基金资助项目(31271030)
关键词 miR-23a miR-30a 炎症 骨缺失 miR-23a miR-30a inflammation bone tissue destruction
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