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机构地区:[1]口腔基础医学省部共建国家重点实验室培育基地和口腔生物医学教育部重点实验室,武汉大学口腔医学院,武汉430079 [2]十堰市太和医院口腔科,十堰422000
出 处:《国际口腔医学杂志》2014年第5期598-602,共5页International Journal of Stomatology
基 金:国家自然科学基金(30973314)
摘 要:研究过氧化物酶增生物激活受体(PPAR)γ及其分子机制,可揭示牙周病与系统性疾病间的关系。PPARγ有6个区域,4个功能结构域,可在配体的作用下调控诸多靶基因转录,从而参与动脉粥样硬化的发病进程,调节血糖血脂水平,改善胰岛素抵抗,是牙周干细胞向脂肪细胞转化的转录因子。PPARγ通过抑制促炎递质基因的表达,影响炎性细胞中的信号通路进而抑制炎症进程。PPARγ可通过经典和非经典无翅型小鼠乳房肿瘤病毒整合位点家族和β-连环蛋白通路增加脂肪细胞的分化,进而抑制成骨细胞分化和促进破骨细胞分化。PPARγ配体作用于炎性转录途径中多个环节,抑制细胞因子、趋化因子和黏附因子等基因表达,对牙周炎有一定的保护作用。脂多糖(LPS)是导致牙槽骨丧失的慢性进展性炎症的主要因子,PPARγ激动剂可降低LPS诱导的蛋白激酶B的磷酸化,抑制牙周炎的炎性骨吸收。The study of peroxisomal proliferator activated receptor(PPAR)γ and the its molecular mechanism can reveal the relationship between periodontitis and systemic diseases. PPARγ, which is composed of six areas and four function structural domains, can regulate a variety of nucleus target genes upon being activated by its ligand. Thus, PPARγ participates in atherosclerosis, regulates the blood glucose and lipids, and improves insulin resistance. PPARγ, is a transcription factor that can convert periodontal stem cells into adipocyte. It can also affect the signaling pathways in inflammatory cells and inhibit the inflammatory process. PPARγ, can promote fat cell differentiation, inhibit osteoblast differentiation, and promote osteoclast differentiation through the classic and non-classic wingless-type mice mammary tumor virus integration site family and β-serial protein pathways. PPARγ exerts a protective effect on periodontitis by inhibiting the gene expression of cytokines, chemokines, and the adhesion factor in the multiple links of inflammatory transcription. Lipopolysaccharide(LPS) is the main factor in chronic progressive inflammatory alveolar bone loss. The PPARγ agonist can decrease the LPS-induced phosphorylation of protein kinase B and thus inhibits the inflammatory bone resorption of periodontitis.
关 键 词:过氧化物酶增生物激活受体γ 牙周炎 骨代谢
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