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论文摘要

蓬乱蛋白2在高脂血症大鼠种植体周围早期表达的实验研究

Disheveled 2 around the implant at an early stage of hyperlipidemic rats

作者:董晓菲, 王会, 蓝菁

Author:Xiaofei Dong, Hui Wang, Jing Lan

收稿日期:2017-07-10          年卷(期)页码:2018,36(1):82-82-86

期刊名称:华西口腔医学杂志

Journal Name:West China Journal of Stomatology

关键字:高脂血症,骨改建,蓬乱蛋白2,Wnt信号通路,

Key words:hyperlipidemia,bone remodeling,disheveled 2,Wnt signal pathway,

基金项目:[基金项目] 国家自然科学基金(81671025);山东省科技发展计划(2015GSF118186)

中文摘要

目的 研究蓬乱蛋白2(Dvl2)在高脂血症大鼠种植体周围早期的表达。方法 24只雄性Wistar大鼠,随机均分为实验组和对照组,分别给予高脂和普通饲料。8周后,检测大鼠血脂水平并于股骨干骺端植入种植体,术后1、3、5 d处死,获得种植体周围骨组织。采用亚甲基蓝-酸性品红染色观察种植体-骨界面,采用实时荧光定量聚合酶链反应(RT-PCR)检测Runt相关转录因子2(Runx2)、组织蛋白酶K(CatK)和Dvl2的表达,免疫印迹和免疫共沉淀法检测Dvl2、磷酸化Dvl2和泛素化Dvl2的表达。结果 与对照组相比,实验组的成骨细胞、Runx2、Dvl2和磷酸化Dvl2减少(P<0.05),而破骨细胞、CatK和泛素化Dvl2增多(P<0.05)。结论 高脂血症可能通过上调Dvl2及磷酸化、下调泛素化而抑制种植体周围早期骨改建。

英文摘要

ObjectiveThis study aims to investigate the expression of disheveled 2 (Dvl2) around the implant of hyperli-pidemic rats at an early stage after the implantation.MethodsA total of 24 Wistar rats were divided equally into the experi-mental group fed with high-fat diet group and control group fed with a normal diet. After 8 weeks, the serum lipid levels were detected, and rats received implants in the femur metaphysis. Rats were sacrificed at 1, 3, and 5 days after implantation, and the bones around implants were obtained. Methylene blue-acid fuchsin staining was performed to observe the implant-bone interface. Real-time polymerase chain reaction was performed on runt-related transcription factor 2 (Runx2), cathepsin K (CatK), and Dvl2. Dvl2 Western blot or immunoprecipitation, phosphorylation, and ubiquitination were also conducted.ResultsIn the experimental group, less osteoblasts, lower expression of Runx2 and Dvl2, and lower Dvl2 phosphorylation (P<0 .05) than those of the control group were observed; furthermore, the catk expression and dvl2 ubiquitination were higher than those in the control group (P<0 .05).ConclusionHyperlipidemia may suppress bone remodeling around the implant at an early stage by Dvl2 down-regulation, phosphorylation, and up-regulated ubiquitination.

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