Functions and mechanisms of green tea catechins in regulating bone remodeling.

Functions and mechanisms of green tea catechins in regulating bone remodeling.
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DOI:
10.2174/13894501113146660216
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发表时间:
2013-11
影响因子:
3.2
通讯作者:
Chwan-Li Shen;I. Kwun;Shu Wang;H. Mo;Lixia Chen;M. Jenkins;G. Brackee;Chung-Hwan Chen;M. Chyu
Chwan-Li Shen;I. Kwun;Shu Wang;H. Mo;Lixia Chen;M. Jenkins;G. Brackee;Chung-Hwan Chen;M. Chyu
中科院分区:
医学4区
文献类型:
--
作者:
Chwan-Li Shen;I. Kwun;Shu Wang;H. Mo;Lixia Chen;M. Jenkins;G. Brackee;Chung-Hwan Chen;M. Chyu

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骨质疏松症是由骨重建失衡引起的,骨重建是一个涉及骨形成成骨细胞和骨吸收破骨细胞的过程。过量的活性氧和炎症反应可刺激破骨细胞的分化和功能,同时通过细胞外信号调节激酶(ERK)、ERK依赖的核因子-κB和Wnt/β-catenin信号通路诱导成骨细胞凋亡并抑制成骨细胞的增殖和分化。绿色茶儿茶素(GTC)具有抗氧化、抗炎作用,可通过调节信号通路促进成骨细胞生成、抑制破骨细胞生成,并刺激间充质干细胞分化为成骨细胞而非脂肪细胞。本文综述了GTC的药代动力学和代谢,其在体外和体内研究中证明的骨保护活性,以及支持这些临床前研究结果的有限临床研究。鉴于骨质疏松症造成的身体、经济和社会负担,在其临床应用之前,GTC等易于获得和负担得起的预防措施值得进一步的临床研究。
Osteoporosis is caused by an imbalance in bone remodeling, a process involving bone-building osteoblasts and bone-resorptive osteoclasts. Excessive reactive oxygen species and inflammatory responses have been shown to stimulate differentiation and function of osteoclasts while inducing osteoblast apoptosis and suppressing osteoblastic proliferation and differentiation via extracellular signal-regulated kinases (ERK), ERK-dependent nuclear factor-κB and Wnt/β-catenin signaling pathways. The anti-oxidant and anti-inflammatory green tea catechins (GTC) have been shown to promote osteoblastogenesis, suppress osteoclastogenesis and stimulate the differentiation of mesenchymal stem cells into osteoblasts rather than adipocytes by modulating the signaling pathways. This paper reviews the pharmacokinetics and metabolism of GTC, their bone-protective activities evidenced in in vitro and in vivo studies, and the limited clinical studies supporting these preclinical findings. In light of the physical, economical, and social burdens due to osteoporosis, easily accessible and affordable preventive measures such as GTC deserves further clinical studies prior to its clinical application.