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首页> 外文期刊>Journal of Cellular Physiology >Alpha-Lipoic Acid Promotes Osteoblastic Formation in H2O2-Treated MC3T3-E1 Cells and Prevents Bone Loss in Ovariectomized Rats
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Alpha-Lipoic Acid Promotes Osteoblastic Formation in H2O2-Treated MC3T3-E1 Cells and Prevents Bone Loss in Ovariectomized Rats

机译：α硫辛酸能促进成骨细胞的形成在H2O2-Treated MC3T3-E1细胞和防止骨损失切除卵巢的老鼠

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摘要

Alpha-lipoic acid (ALA), a naturally occurring compound and dietary supplement, has been established as a potent antioxidant that is a strong scavenger of free radicals. Recently, accumulating evidences has indicated the relationship between oxidative stress and osteoporosis (OP). Some studies have investigated the possible beneficial effects of ALA on OP both in vivo and in vitro; however, the precise mechanism(s) underlying the bone-protective action of ALA remains unclear. Considering this, we focused on the anti-oxidative capacity of ALA to exert bone-protective effects in vitro and in vivo. In the present study, the effects of ALA on osteoblastic formation in H2O2-treated MC3T3-E1 pre-osteoblasts and ovariectomy (OVX)-induced bone loss in rats were investigated. The results showed that ALA promoted osteoblast differentiation, mineralization and maturation and inhibited osteoblast apoptosis, thus increasing the OPG/receptor activator of nuclear factor-B (NF-B) ligand (RANKL) ratio and leading to enhanced bone formation in vitro and inhibited bone loss in vivo. Further study revealed that ALA exerted its bone-protective effects by inhibiting reactive oxygen species (ROS) generation by down-regulating Nox4 gene expression and protein synthesis and attenuating the transcriptional activation of NF-B. In addition, ALA might exert its bone-protective effects by activating the Wnt/Lrp5/-catenin signaling pathway. Taken together, the present study indicated that ALA promoted osteoblastic formation in H2O2-treated MC3T3-E1 cells and prevented OVX-induced bone loss in rats by regulating Nox4/ROS/NF-B and Wnt/Lrp5/-catenin signaling pathways, which provided possible mechanisms of bone-protective effects in regulating osteoblastic formation and preventing bone loss. Taken together, the results suggest that ALA may be a candidate for clinical OP treatment. J. Cell. Physiol. 230: 2184-2201, 2015. (c) 2015 Wiley Periodicals, Inc.
机译：α硫辛酸(ALA),一个自然发生的化合物和膳食补充剂作为一种强有力的抗氧化剂,是建立较强的自由基的清道夫。积累的证据表明氧化应激和之间的关系骨质疏松症(OP)。阿拉巴马州的可能的有利影响OP体内和体外;机制(s)潜在的预防骨质疏松阿拉巴马州的作用仍不清楚。我们专注于阿拉巴马州的氧化能力施加在体外和预防骨质疏松的影响vivo成骨细胞的形成H2O2-treated MC3T3-E1pre-osteoblasts和卵巢切除术(OVX)全身老鼠的骨质流失。表明,阿拉巴马州促进成骨细胞分化、矿化和成熟和抑制成骨细胞凋亡,从而增加的功能/受体激活核因子b (NF-B)配体(RANKL)比率和领导增强体外骨形成抑制骨质流失体内。阿拉巴马州对其预防骨质疏松的影响抑制活性氧(ROS)一代显示Nox4基因表达和蛋白质合成和衰减NF-B的转录激活。此外,阿拉巴马州可能发挥其预防骨质疏松通过激活Wnt / Lrp5 /连环蛋白的影响信号通路。研究表明,阿拉巴马州促进成骨细胞的形成H2O2-treated MC3T3-E1细胞预防OVX-induced老鼠的骨质流失调节Nox4 / ROS / NF-B和Wnt / Lrp5 /连环蛋白信号通路,提供可能预防骨质疏松的作用机制调节成骨细胞的形成和预防骨质流失。阿拉巴马州可能适合临床OP治疗。2015.

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