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N-acetylcysteine prevents orchiectomy-induced osteoporosis by inhibiting oxidative stress and osteocyte senescence.N-乙酰半胱氨酸通过抑制氧化应激和骨细胞衰老来预防睾丸切除诱导的骨质疏松症。
Am J Transl Res. 2019 Jul 15;11(7):4337-4347. eCollection 2019.
2
Suppression effect of N-acetylcysteine on bone loss in ovariectomized mice.N-乙酰半胱氨酸对去卵巢小鼠骨质流失的抑制作用。
Am J Transl Res. 2020 Mar 15;12(3):731-742. eCollection 2020.
3
CoQ10 suppression of oxidative stress and cell senescence increases bone mass in orchiectomized mice.辅酶Q10对氧化应激和细胞衰老的抑制作用可增加去势小鼠的骨量。
Am J Transl Res. 2020 Aug 15;12(8):4314-4325. eCollection 2020.
4
Pyrroloquinoline Quinone Prevents Estrogen Deficiency-Induced Osteoporosis by Inhibiting Oxidative Stress and Osteocyte Senescence.吡咯并喹啉醌通过抑制氧化应激和骨细胞衰老预防雌激素缺乏诱导的骨质疏松症。
Int J Biol Sci. 2019 Jan 1;15(1):58-68. doi: 10.7150/ijbs.25783. eCollection 2019.
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Pyrroloquinoline quinone prevents testosterone deficiency-induced osteoporosis by stimulating osteoblastic bone formation and inhibiting osteoclastic bone resorption.吡咯喹啉醌通过刺激成骨细胞骨形成和抑制破骨细胞骨吸收来预防睾酮缺乏诱导的骨质疏松症。
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本文引用的文献

1
Pyrroloquinoline quinone prevents knee osteoarthritis by inhibiting oxidative stress and chondrocyte senescence.吡咯喹啉醌通过抑制氧化应激和软骨细胞衰老来预防膝骨关节炎。
Am J Transl Res. 2019 Mar 15;11(3):1460-1472. eCollection 2019.
2
1,25-Dihydroxyvitamin D exerts an antiaging role by activation of Nrf2-antioxidant signaling and inactivation of p16/p53-senescence signaling.1,25-二羟维生素 D 通过激活 Nrf2-抗氧化信号和失活 p16/p53-衰老信号来发挥抗衰老作用。
Aging Cell. 2019 Jun;18(3):e12951. doi: 10.1111/acel.12951. Epub 2019 Mar 24.
3
Pyrroloquinoline Quinone Prevents Estrogen Deficiency-Induced Osteoporosis by Inhibiting Oxidative Stress and Osteocyte Senescence.吡咯并喹啉醌通过抑制氧化应激和骨细胞衰老预防雌激素缺乏诱导的骨质疏松症。
Int J Biol Sci. 2019 Jan 1;15(1):58-68. doi: 10.7150/ijbs.25783. eCollection 2019.
4
Osteoporosis: a clinical and pharmacological update.骨质疏松症:临床与药理学更新。
Clin Rheumatol. 2019 Feb;38(2):385-395. doi: 10.1007/s10067-018-4370-1. Epub 2018 Dec 12.
5
[Senescent cells: a target in osteo-articular diseases].[衰老细胞:骨关节疾病的一个靶点]
Med Sci (Paris). 2018 Jun-Jul;34(6-7):547-553. doi: 10.1051/medsci/20183406014. Epub 2018 Jul 31.
6
Suppression Effect of Astaxanthin on Osteoclast Formation In Vitro and Bone Loss In Vivo.虾青素对体外破骨细胞形成和体内骨丢失的抑制作用。
Int J Mol Sci. 2018 Mar 19;19(3):912. doi: 10.3390/ijms19030912.
7
Gender differences in anti-osteoporosis drug treatment after osteoporotic fractures.骨质疏松性骨折后抗骨质疏松药物治疗的性别差异。
J Bone Miner Metab. 2019 Jan;37(1):134-141. doi: 10.1007/s00774-018-0904-5. Epub 2018 Mar 13.
8
Effect and mechanism of pyrroloquinoline quinone on anti-osteoporosis in Bmi-1 knockout mice-Anti-oxidant effect of pyrroloquinoline quinone.吡咯喹啉醌对Bmi-1基因敲除小鼠抗骨质疏松的作用及机制——吡咯喹啉醌的抗氧化作用
Am J Transl Res. 2017 Oct 15;9(10):4361-4374. eCollection 2017.
9
Corrigendum: Targeting cellular senescence prevents age-related bone loss in mice.勘误:靶向细胞衰老可预防小鼠年龄相关性骨质流失。
Nat Med. 2017 Nov 7;23(11):1384. doi: 10.1038/nm1117-1384c.
10
Old age causes de novo intracortical bone remodeling and porosity in mice.老年导致小鼠皮质内新骨重塑和多孔性。
JCI Insight. 2017 Sep 7;2(17). doi: 10.1172/jci.insight.93771.

N-乙酰半胱氨酸通过抑制氧化应激和骨细胞衰老来预防睾丸切除诱导的骨质疏松症。

N-acetylcysteine prevents orchiectomy-induced osteoporosis by inhibiting oxidative stress and osteocyte senescence.

作者信息

Chen Lulu, Wang Guantong, Wang Qinjue, Liu Quan, Sun Qiang, Chen Lulu

机构信息

Department of Anatomy, Histology and Embryology, Nanjing Medical University Nanjing 211166, Jiangsu, China.

Key Laboratory for Aging and Disease, Histology and Embryology, Nanjing Medical University Nanjing 211166, Jiangsu, China.

出版信息

Am J Transl Res. 2019 Jul 15;11(7):4337-4347. eCollection 2019.

PMID:31396339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6684909/
Abstract

Oxidative stress is associated with many diseases and has been found to induce DNA damage and cellular senescence. Numerous evidences support the detrimental effects of oxidative stress or cellular senescence on skeletal homeostasis. N-acetylcysteine (NAC) is a powerful antioxidant. However, it is unclear whether NAC can suppress orchiectomy (ORX)-induced osteoporosis by inhibiting oxidative stress and osteocyte senescence. In this study, ORX mice were supplemented with/without NAC, and were compared with each other and with sham-operated mice. Our results showed that NAC could prevent ORX-induced osteoporosis by inhibiting oxidative stress, DNA damage, osteocyte senescence and senescence-associated secretory phenotype (SASP), subsequently stimulating osteoblastic bone formation and inhibiting osteoclastic bone resorption. The results from this study suggest that NAC could be considered as a potential therapeutic agent for prevention and treatment of osteoporosis caused by testosterone deficiency.

摘要

氧化应激与多种疾病相关,并且已发现其可诱导DNA损伤和细胞衰老。大量证据支持氧化应激或细胞衰老对骨骼稳态的有害影响。N-乙酰半胱氨酸(NAC)是一种强大的抗氧化剂。然而,目前尚不清楚NAC是否能够通过抑制氧化应激和骨细胞衰老来抑制去势(ORX)诱导的骨质疏松症。在本研究中,对去势小鼠补充或不补充NAC,并将其相互比较,同时与假手术小鼠进行比较。我们的结果表明,NAC可通过抑制氧化应激、DNA损伤、骨细胞衰老和衰老相关分泌表型(SASP),随后刺激成骨细胞骨形成并抑制破骨细胞骨吸收,从而预防去势诱导的骨质疏松症。本研究结果表明,NAC可被视为预防和治疗由睾酮缺乏引起的骨质疏松症的潜在治疗药物。