• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

硅肺会降低大鼠的骨密度。

Silicosis decreases bone mineral density in rats.

机构信息

Medical Research Center, North China University of Science and Technology, Tangshan, China.

College of Traditional Chinese Medicine, North China University of Science and Technology, Tangshan, China.

出版信息

Toxicol Appl Pharmacol. 2018 Jun 1;348:117-122. doi: 10.1016/j.taap.2018.04.023. Epub 2018 Apr 19.

DOI:10.1016/j.taap.2018.04.023
PMID:29680408
Abstract

Silicosis is the most common occupational lung disease in China, and is associated with a variety of complications, many of which are poorly understood. For example, recent data indicate that silicosis associates with the development of osteopenia, and in some cases this bone loss is severe, meeting criteria for osteoporosis. Although many factors are likely to contribute to this relationship, including a sedentary lifestyle in patients with advanced silicotic lung disease, we hypothesized that silica might directly reduce bone mineral density. In the present study, six Wistar rats were exposed to silica for 24 weeks in order to induce pulmonary silicosis and examine the relationship to bone mineral density. As expected, all rats exposed to silica developed severe pulmonary fibrosis, as manifested by the formation of innumerable silicotic nodules and the deposition of large amounts of interstitial collagen. Moreover, micro-CT results showed that bone mineral density (BMD) was also significantly reduced in rats exposed to silica when compared control animals and this associated with a modest reduction in serum calcium and 25-hydroxyvitamin D levels. In addition, we found that decreased BMD was also linked to increased osteoclast activity as well as fibrosis-like changes, and to the deposition of silica within bone marrow. In summary, our findings support the hypothesis that silicosis reduces bone mineral density and provide support for ongoing investigations into the mechanisms causing osteopenia in silicosis patients.

摘要

矽肺是中国最常见的职业性肺部疾病,与多种并发症相关,其中许多并发症的发病机制尚未完全阐明。例如,最近的数据表明矽肺与骨质疏松症的发生有关,在某些情况下,这种骨质流失非常严重,符合骨质疏松症的诊断标准。尽管许多因素可能与这种相关性有关,包括晚期矽肺患者的久坐生活方式,但我们假设二氧化硅可能直接降低骨密度。在本研究中,我们将 6 只 Wistar 大鼠暴露于二氧化硅中 24 周,以诱导肺部矽肺,并研究其与骨密度的关系。正如预期的那样,所有暴露于二氧化硅的大鼠均发展为严重的肺纤维化,表现为无数矽结节的形成和大量间质胶原的沉积。此外,微 CT 结果显示,与对照组动物相比,暴露于二氧化硅的大鼠的骨密度(BMD)也显著降低,同时血清钙和 25-羟维生素 D 水平也略有降低。此外,我们发现,BMD 的降低还与破骨细胞活性的增加、纤维化样改变以及骨髓内二氧化硅的沉积有关。总之,我们的研究结果支持矽肺降低骨密度的假说,并为进一步研究矽肺患者骨质疏松症的发病机制提供了依据。

相似文献

1
Silicosis decreases bone mineral density in rats.硅肺会降低大鼠的骨密度。
Toxicol Appl Pharmacol. 2018 Jun 1;348:117-122. doi: 10.1016/j.taap.2018.04.023. Epub 2018 Apr 19.
2
[Anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline in lung of rat with silicosis].N-乙酰丝氨酰-天冬氨酰-赖氨酰-脯氨酸对矽肺大鼠肺组织的抗纤维化作用
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2008 Jul;26(7):401-5.
3
Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis.二氧化硅诱导肺纤维化中的破骨细胞样细胞。
Sci Adv. 2024 Jul 12;10(28):eadl4913. doi: 10.1126/sciadv.adl4913. Epub 2024 Jul 10.
4
Profiling long non-coding RNA changes in silica-induced pulmonary fibrosis in rat.分析二氧化硅诱导的大鼠肺纤维化中长非编码 RNA 的变化。
Toxicol Lett. 2019 Aug;310:7-13. doi: 10.1016/j.toxlet.2019.04.003. Epub 2019 Apr 9.
5
Repeated Silica exposures lead to Silicosis severity via PINK1/PARKIN mediated mitochondrial dysfunction in mice model.反复的二氧化硅暴露通过 PINK1/PARKIN 介导的线粒体功能障碍导致小鼠模型中矽肺的严重程度。
Cell Signal. 2024 Sep;121:111272. doi: 10.1016/j.cellsig.2024.111272. Epub 2024 Jun 27.
6
Evaluation of bone mineral density and 25-hydroxyvitamin D levels in subjects with silica exposure.二氧化硅暴露受试者的骨密度和25-羟基维生素D水平评估。
Environ Health Prev Med. 2016 May;21(3):149-53. doi: 10.1007/s12199-016-0509-3. Epub 2016 Jan 29.
7
Pulmonary hypertension and vascular remodeling in mice exposed to crystalline silica.暴露于结晶二氧化硅的小鼠中的肺动脉高压和血管重塑。
Respir Res. 2016 Nov 28;17(1):160. doi: 10.1186/s12931-016-0478-5.
8
Therapeutic effects of scavenger receptor MARCO ligand on silica-induced pulmonary fibrosis in rats.MARCO 配体对二氧化硅诱导的大鼠肺纤维化的治疗作用。
Toxicol Lett. 2019 Sep 1;311:1-10. doi: 10.1016/j.toxlet.2019.04.026. Epub 2019 Apr 24.
9
Upregulated miR-29c suppresses silica-induced lung fibrosis through the Wnt/β-catenin pathway in mice.上调的miR-29c通过Wnt/β-连环蛋白通路抑制小鼠二氧化硅诱导的肺纤维化。
Hum Exp Toxicol. 2018 Sep;37(9):944-952. doi: 10.1177/0960327117741750. Epub 2017 Dec 8.
10
Low-level lifetime exposure to cadmium decreases skeletal mineralization and enhances bone loss in aged rats.镉的低水平终生暴露会降低老年大鼠的骨骼矿化并加剧骨质流失。
Bone. 2004 Nov;35(5):1180-91. doi: 10.1016/j.bone.2004.07.010.

引用本文的文献

1
Correlation between occupational hazard exposure and abnormal bone mineral density in steelworkers.钢铁工人职业危害暴露与骨密度异常之间的相关性
BMC Public Health. 2025 Apr 16;25(1):1431. doi: 10.1186/s12889-025-22713-4.
2
OC-STAMP is a potential biomarker and therapeutic target for Silicosis: an exploratory investigation.OC-STAMP是矽肺的潜在生物标志物和治疗靶点:一项探索性研究。
J Transl Med. 2025 Feb 21;23(1):214. doi: 10.1186/s12967-024-05981-3.
3
The Role of Trace Elements and Minerals in Osteoporosis: A Review of Epidemiological and Laboratory Findings.
微量元素和矿物质在骨质疏松症中的作用:流行病学和实验室研究结果综述。
Biomolecules. 2023 Jun 17;13(6):1006. doi: 10.3390/biom13061006.
4
Minute Cellular Nodules as Early Lesions in Rats with Silica Exposure via Inhalation.微小细胞结节作为大鼠经吸入暴露于二氧化硅后的早期病变
Vet Sci. 2022 May 25;9(6):251. doi: 10.3390/vetsci9060251.
5
Thalidomide Alleviates Pulmonary Fibrosis Induced by Silica in Mice by Inhibiting ER Stress and the TLR4-NF-κB Pathway.沙利度胺通过抑制内质网应激和 TLR4-NF-κB 通路缓解二氧化硅诱导的小鼠肺纤维化。
Int J Mol Sci. 2022 May 18;23(10):5656. doi: 10.3390/ijms23105656.
6
Early Identification, Accurate Diagnosis, and Treatment of Silicosis.矽肺的早期识别、准确诊断和治疗。
Can Respir J. 2022 Apr 25;2022:3769134. doi: 10.1155/2022/3769134. eCollection 2022.
7
Activation of canonical inflammasome complex by acute silica exposure in experimental rat model.在实验大鼠模型中,急性二氧化硅暴露激活经典炎性小体复合物。
Toxicol Res (Camb). 2022 Jan 8;11(1):162-168. doi: 10.1093/toxres/tfab127. eCollection 2022 Feb.
8
Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment.硅诱导的肺巨噬细胞糖酵解重编程及 Ac-SDKP 治疗逆转矽肺。
Int J Mol Sci. 2021 Sep 17;22(18):10063. doi: 10.3390/ijms221810063.
9
OC-STAMP Overexpression Drives Lung Alveolar Epithelial Cell Type II Senescence in Silicosis.OC-STAMP 过表达驱动矽肺中肺泡上皮细胞 II 型衰老。
Oxid Med Cell Longev. 2021 Aug 14;2021:4158495. doi: 10.1155/2021/4158495. eCollection 2021.
10
Ac-SDKP Attenuates Activation of Lung Macrophages and Bone Osteoclasts in Rats Exposed to Silica by Inhibition of TLR4 and RANKL Signaling Pathways.N-乙酰-S-天冬氨酰-L-赖氨酰-L-脯氨酰-L-缬氨酸通过抑制Toll样受体4(TLR4)和核因子κB受体激活蛋白配体(RANKL)信号通路减轻二氧化硅暴露大鼠肺巨噬细胞和骨破骨细胞的激活
J Inflamm Res. 2021 Apr 27;14:1647-1660. doi: 10.2147/JIR.S306883. eCollection 2021.