Partial Protection by Dietary Antioxidants Against Ethanol-Induced Osteopenia and Changes in Bone Morphology in Female Mice.
Partial Protection by Dietary Antioxidants Against Ethanol-Induced Osteopenia and Changes in Bone Morphology in Female Mice.
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DOI：
10.1111/acer.13284
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发表时间：
2017-01
期刊：
影响因子：
--
通讯作者：
Ronis MJ
中科院分区：
文献类型：
--
作者：
Alund AW;Mercer KE;Pulliam CF;Suva LJ;Chen JR;Badger TM;Ronis MJ
慢性饮酒通过增加破骨细胞活性和降低成骨细胞活性来减少骨累积，从而导致骨折风险增加和骨质疏松症风险升高。我们已经证明这种机制涉及由NADPH氧化酶（NOX）产生的活性氧（ROS）的产生。假设不同的膳食抗氧化剂n -乙酰半胱氨酸（NAC, 1.2mg/kg/d）和α-生育酚（VitE, 60 mg/kg/d）能够减弱慢性酒精摄入引起的nox介导的ROS对骨骼的影响。为了研究这些抗氧化剂的作用，雌性小鼠连续8周接受含乙醇（EtOH）和不含抗氧化剂的Lieber DeCarli液体饮食。与成对饲养（PF）和PF+抗氧化剂组相比，EtOH和EtOH+抗氧化剂组胫骨皮质骨矿物质密度均降低（P<0.05）。然而，两种抗氧化剂均对小鼠骨小梁丢失有显著保护作用（P<0.05）。显微ct分析显示骨体积（BV/TV）和小梁数量（Tb）明显减少。N) (P<0.05)， EtOH的小梁间距（Tb.Sp）较PF显著增加（P<0.05）。相比之下，EtOH+NAC和EtOH+α-生育酚与各自的PF对照组没有统计学差异。对胫骨离体组织切片进行硝基酪氨酸染色，硝基酪氨酸是细胞内ROS损伤的指标，饲喂EtOH的小鼠胫骨的染色明显高于PF对照组。EtOH处理显著增加每mm骨髓脂肪细胞数量和骨脂肪细胞标志物aP2的mRNA表达。只有NAC能够将骨髓脂肪细胞的数量减少到PF水平。EtOH喂养的小鼠骨长度减少（P<0.05），生长板内增殖软骨细胞数量减少。NAC和维生素E可阻止这一现象（P<0.05）。这些数据表明，酒精对骨骼的病理影响不仅仅是减少骨量，而且表明在这些剂量下，膳食抗氧化剂NAC和α-生育酚对骨骼转换和骨骼形态的影响具有部分保护作用。
Chronic alcohol consumption leads to increased fracture risk and an elevated risk of osteoporosis by decreasing bone accrual through increasing osteoclast activity and decreasing osteoblast activity. We have shown that this mechanism involves the generation of reactive oxygen species (ROS) produced by NADPH oxidases (NOX). It was hypothesized that different dietary antioxidants, N-acetyl cysteine (NAC, 1.2mg/kg/d) and α-tocopherol (VitE, 60 mg/kg/d)) would be able to attenuate the NOX-mediated ROS effects on bone due to chronic alcohol intake. To study the effects of these antioxidants, female mice received a Lieber DeCarli liquid diet containing ethanol (EtOH) with or without additional antioxidant for 8 weeks. Tibias displayed decreased cortical bone mineral density in both the EtOH and EtOH+antioxidant groups compared to pair-fed (PF) and PF+antioxidant groups (P<0.05). However, there was significant protection from trabecular bone loss in mice fed either antioxidant (P<0.05). MicroCT analysis demonstrated a significant decrease in bone volume (BV/TV) and trabecular number (Tb.N) (P<0.05), along with a significant increase in trabecular spacing (Tb.Sp) in the EtOH compared to PF (P<0.05). In contrast, the EtOH+NAC and EtOH+α-tocopherol did not statistically differ from their respective PF controls. Ex vivo histological sections of tibias were stained for nitrotyrosine, an indicator of intracellular damage by ROS, and tibias from mice fed EtOH exhibited significantly more staining than PF controls. EtOH treatment significantly increased the number of marrow adipocytes per mm as well as mRNA expression of aP2, an adipocyte marker in bone. Only NAC was able to reduce the number of marrow adipocytes to PF levels. EtOH fed mice exhibited reduced bone length (P<0.05) and had a reduced number of proliferating chondrocytes within the growth plate. NAC and Vitamin E prevented this (P<0.05). These data show that alcohol’s pathological effects on bone extend beyond decreasing bone mass and suggest a partial protective effect of the dietary antioxidants NAC and α-tocopherol at these doses with regard to alcohol effects on bone turnover and bone morphology.
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影响因子：
2.8
作者：
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通讯作者：
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影响因子：
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作者：
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DOI：
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发表时间：
2014-01-01
期刊：
AGING: FACTS AND THEORIES
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作者：
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DOI：
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发表时间：
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期刊：
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
影响因子：
--
作者：
Chen JR;Lazarenko OP;Haley RL;Blackburn ML;Badger TM;Ronis MJ
通讯作者：
Ronis MJ