中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
15期
2405-2409
,共5页
组织构建%骨组织工程%甲状旁腺激素%骨代谢%成骨细胞%细胞因子%国家自然科学基金
組織構建%骨組織工程%甲狀徬腺激素%骨代謝%成骨細胞%細胞因子%國傢自然科學基金
조직구건%골조직공정%갑상방선격소%골대사%성골세포%세포인자%국가자연과학기금
Subject headings:Thyroid Hormones%Osteoblasts%Cytokines
背景：骨质疏松是表现为骨矿化密度低下以及骨微结构不良，从而易导致骨折发生的一种疾病，常并发口腔表征。甲状旁腺激素是在骨形成以及钙盐沉积过程中的重要调节因素，间歇性的甲状旁腺激素注射已经被广泛的证实可以促进骨质的形成。<br> 目的：探讨甲状旁腺激素增强骨密度以及调节骨形成代谢的可能细胞及分子机制。<br> 方法：由第一作者用计算机检索全国期刊全文数据库(CNKI)，Medline 数据库，检索词分别为“甲状旁腺激素，骨质疏松，成骨细胞，骨形成”和“Parathyroid hormone；osteoporosis；osteoblast；osteogenesis”。从甲状旁腺激素对成骨细胞分化、增殖的作用，甲状旁腺激素对成骨细胞凋亡的作用，甲状旁腺激素与 Wnt/β-catenin通路以及其他细胞因子的作用关系3个方面进行总结。按纳入和排除标准对文献进行筛选，共纳入41篇文章。结果与结论：甲状旁腺激素作用于甲状旁腺激素Ⅰ型受体，触发经典的G蛋白信号通路。甲状旁腺激素主要通过蛋白激酶信号A通路，调节其下游反应蛋白。间歇性使用甲状旁腺激素提高成骨细胞增殖能力，提高成骨细胞骨转录因子 runx2和骨钙素(mRNA 和蛋白水平)的表达，通过对抗氧化应激抑制成骨细胞凋亡，从而促进成骨。
揹景：骨質疏鬆是錶現為骨礦化密度低下以及骨微結構不良，從而易導緻骨摺髮生的一種疾病，常併髮口腔錶徵。甲狀徬腺激素是在骨形成以及鈣鹽沉積過程中的重要調節因素，間歇性的甲狀徬腺激素註射已經被廣汎的證實可以促進骨質的形成。<br> 目的：探討甲狀徬腺激素增彊骨密度以及調節骨形成代謝的可能細胞及分子機製。<br> 方法：由第一作者用計算機檢索全國期刊全文數據庫(CNKI)，Medline 數據庫，檢索詞分彆為“甲狀徬腺激素，骨質疏鬆，成骨細胞，骨形成”和“Parathyroid hormone；osteoporosis；osteoblast；osteogenesis”。從甲狀徬腺激素對成骨細胞分化、增殖的作用，甲狀徬腺激素對成骨細胞凋亡的作用，甲狀徬腺激素與 Wnt/β-catenin通路以及其他細胞因子的作用關繫3箇方麵進行總結。按納入和排除標準對文獻進行篩選，共納入41篇文章。結果與結論：甲狀徬腺激素作用于甲狀徬腺激素Ⅰ型受體，觸髮經典的G蛋白信號通路。甲狀徬腺激素主要通過蛋白激酶信號A通路，調節其下遊反應蛋白。間歇性使用甲狀徬腺激素提高成骨細胞增殖能力，提高成骨細胞骨轉錄因子 runx2和骨鈣素(mRNA 和蛋白水平)的錶達，通過對抗氧化應激抑製成骨細胞凋亡，從而促進成骨。
배경：골질소송시표현위골광화밀도저하이급골미결구불량，종이역도치골절발생적일충질병，상병발구강표정。갑상방선격소시재골형성이급개염침적과정중적중요조절인소，간헐성적갑상방선격소주사이경피엄범적증실가이촉진골질적형성。<br> 목적：탐토갑상방선격소증강골밀도이급조절골형성대사적가능세포급분자궤제。<br> 방법：유제일작자용계산궤검색전국기간전문수거고(CNKI)，Medline 수거고，검색사분별위“갑상방선격소，골질소송，성골세포，골형성”화“Parathyroid hormone；osteoporosis；osteoblast；osteogenesis”。종갑상방선격소대성골세포분화、증식적작용，갑상방선격소대성골세포조망적작용，갑상방선격소여 Wnt/β-catenin통로이급기타세포인자적작용관계3개방면진행총결。안납입화배제표준대문헌진행사선，공납입41편문장。결과여결론：갑상방선격소작용우갑상방선격소Ⅰ형수체，촉발경전적G단백신호통로。갑상방선격소주요통과단백격매신호A통로，조절기하유반응단백。간헐성사용갑상방선격소제고성골세포증식능력，제고성골세포골전록인자 runx2화골개소(mRNA 화단백수평)적표체，통과대항양화응격억제성골세포조망，종이촉진성골。
BACKGROUND:Osteoporosis is characterized by low bone mineral density and/or poor bone microarchitecture leading to an increased risk of fractures. Oral manifestations can be frequently discovered in osteoporosis patients. Osteoporosis therapies have mostly relied on antiresorptive drugs. Parathyroid hormone plays a significant role in osteogenesis and calcium deposition. Intermittent exposure to parathyroid hormone has been widely proved to lead to a net increase in bone formation. <br> OBJECTIVE: To discuss the possibly celular and molecular mechanism of parathyroid hormone in strengthening the bone mineral density and regulating bone formation. <br> METHODS: An online search of CNKI and Medline databases was performed for relevant articles using keywords of “parathyroid hormone; osteoporosis; osteoblast; osteogenesis” in Chinese and English, respectively. Relevant articles were summarized from three aspects: effects of parathyroid hormone on differentiation and proliferation of osteoblasts, effects of parathyroid hormone on osteoblast apoptosis, and the relationship of parathyroid hormone with Wnt/beta-catenin pathway and other cytokines. According to inclusion criteria, 41 articles were retained at last. <br> RESULTS AND CONCLUSION:Parathyroid hormone exerts an effect on parathyroid hormone type I receptor, triggering a classic G protein signaling pathway. Parathyroid hormone mainly works through protein kinase A signaling pathway, adjusting its downstream c-reactive protein. Intermittent use of parathyroid hormone can increase osteoblast proliferation, increase osteoblast runx2 and osteocalcin at mRNA and protein levels, inhibit osteoblast apoptosis by against oxidative stress, so as to promote osteogenesis.
