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β-1肾上腺素能激动剂治疗可减轻松质骨微结构的负面变化，并在废用期间抑制骨细胞凋亡。

Beta-1 adrenergic agonist treatment mitigates negative changes in cancellous bone microarchitecture and inhibits osteocyte apoptosis during disuse.

作者信息

Swift Joshua M, Swift Sibyl N, Allen Matthew R, Bloomfield Susan A

机构信息

Departments of Health and Kinesiology, Texas A & M University, College Station, Texas, United States of America.

Intercollegiate Faculty of Nutrition, Texas A & M University, College Station, Texas, United States of America.

出版信息

PLoS One. 2014 Sep 11;9(9):e106904. doi: 10.1371/journal.pone.0106904. eCollection 2014.

DOI:10.1371/journal.pone.0106904
PMID:25211027
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4161377/
Abstract

The sympathetic nervous system (SNS) plays an important role in mediating bone remodeling. However, the exact role that beta-1 adrenergic receptors (beta1AR) have in this process has not been elucidated. We have previously demonstrated the ability of dobutamine (DOB), primarily a beta1AR agonist, to inhibit reductions in cancellous bone formation and mitigate disuse-induced loss of bone mass. The purpose of this study was to characterize the independent and combined effects of DOB and hindlimb unloading (HU) on cancellous bone microarchitecture, tissue-level bone cell activity, and osteocyte apoptosis. Male Sprague-Dawley rats, aged 6-mos, were assigned to either normal cage activity (CC) or HU (n = 18/group) for 28 days. Animals were administered either daily DOB (4 mg/kg BW/d) or an equal volume of saline (VEH) (n = 9/gp). Unloading resulted in significantly lower distal femur cancellous BV/TV (-33%), Tb.Th (-11%), and Tb.N (-25%) compared to ambulatory controls (CC-VEH). DOB treatment during HU attenuated these changes in cancellous bone microarchitecture, resulting in greater BV/TV (+29%), Tb.Th (+7%), and Tb.N (+21%) vs. HU-VEH. Distal femur cancellous vBMD (+11%) and total BMC (+8%) were significantly greater in DOB- vs. VEH-treated unloaded rats. Administration of DOB during HU resulted in significantly greater osteoid surface (+158%) and osteoblast surface (+110%) vs. HU-VEH group. Furthermore, Oc.S/BS was significantly greater in HU-DOB (+55%) vs. CC-DOB group. DOB treatment during unloading fully restored bone formation, resulting in significantly greater bone formation rate (+200%) than in HU-VEH rats. HU resulted in an increased percentage of apoptotic cancellous osteocytes (+85%), reduced osteocyte number (-16%), lower percentage of occupied osteocytic lacunae (-30%) as compared to CC-VEH, these parameters were all normalized with DOB treatment. Altogether, these data indicate that beta1AR agonist treatment during disuse mitigates negative changes in cancellous bone microarchitecture and inhibits increases in osteocyte apoptosis.

摘要

交感神经系统（SNS）在介导骨重塑过程中发挥着重要作用。然而，β-1肾上腺素能受体（β1AR）在此过程中的确切作用尚未阐明。我们之前已经证明，主要作为β1AR激动剂的多巴酚丁胺（DOB）能够抑制松质骨形成的减少，并减轻废用性骨质流失。本研究的目的是确定DOB和后肢卸载（HU）对松质骨微结构、组织水平骨细胞活性和骨细胞凋亡的独立及联合作用。将6月龄雄性Sprague-Dawley大鼠分为正常笼内活动组（CC）或HU组（每组n = 18只），持续28天。动物每天给予DOB（4 mg/kg体重/天）或等体积的生理盐水（VEH）（每组n = 9只）。与活动对照组（CC-VEH）相比，卸载导致股骨远端松质骨骨体积分数（BV/TV）显著降低（-33%）、骨小梁厚度（Tb.Th）降低（-11%）和骨小梁数量（Tb.N）降低（-25%）。HU期间DOB治疗减轻了松质骨微结构的这些变化，与HU-VEH组相比，BV/TV增加（+29%）、Tb.Th增加（+7%）和Tb.N增加（+21%）。与VEH治疗的卸载大鼠相比，DOB治疗的卸载大鼠股骨远端松质骨体积骨密度（vBMD）显著增加（+11%），总骨矿含量（BMC）显著增加（+8%）。HU期间给予DOB导致类骨质表面显著增加（+158%）和成骨细胞表面显著增加（+110%），与HU-VEH组相比。此外，HU-DOB组的骨表面矿化面积（Oc.S/BS）显著大于CC-DOB组（+55%）。卸载期间DOB治疗完全恢复了骨形成，导致骨形成率显著高于HU-VEH大鼠（+200%）。与CC-VEH组相比，HU导致凋亡性松质骨细胞百分比增加（+85%）、骨细胞数量减少（-A16%）、骨细胞陷窝占有率降低（-L30%），这些参数在DOB治疗后均恢复正常。总之，这些数据表明，废用期间β1AR激动剂治疗可减轻松质骨微结构的负面变化，并抑制骨细胞凋亡增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/788232848c4d/pone.0106904.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/48d8f4e5720f/pone.0106904.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/a4189036be5e/pone.0106904.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/09425f3109ea/pone.0106904.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/62a64dee9c95/pone.0106904.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/9fc80fcf7f6f/pone.0106904.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/788232848c4d/pone.0106904.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/48d8f4e5720f/pone.0106904.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/a4189036be5e/pone.0106904.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/09425f3109ea/pone.0106904.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/62a64dee9c95/pone.0106904.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/9fc80fcf7f6f/pone.0106904.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bb8/4161377/788232848c4d/pone.0106904.g006.jpg

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本文引用的文献

[1]
β-1 adrenergic agonist mitigates unloading-induced bone loss by maintaining formation.

Med Sci Sports Exerc. 2013-9

[2]
β-Adrenergic signaling stimulates osteoclastogenesis via reactive oxygen species.

Am J Physiol Endocrinol Metab. 2012-11-20

[3]
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J Bone Miner Res. 2012-6

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Cancellous bone formation response to simulated resistance training during disuse is blunted by concurrent alendronate treatment.

J Bone Miner Res. 2011-9

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J Bone Miner Res. 2007-5

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