相关实验视频
Updated: May 14, 2025

Estrogen-Like Effect of Bazi Bushen Capsule in Ovariectomized Rats
Published on: April 7, 2023
PPARγ-SMAD6轴介导的骨质分化的抑制与BPS诱导的骨质疏松症有关
Zhenkun Weng1, Xiu Chen2, Jian Jiao2
1State Key Laboratory of Reproductive Medicine and Offspring Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Jiangsu Environmental Health Risk Assessment Engineering Research Center, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Nanjing Medical University, Nanjing 211166, China; Changzhou Second People's Hospital, Changzhou Medical Center, Nanjing Medical University, Changzhou 213004, China.
双S (BPS) 暴露与较低的骨矿物质密度 (BMD) 有关. 这项研究揭示了BPS通过PPARγ-SMAD6通路破坏骨形成,这表明olodanrigan作为BPS诱导的骨质疏松症的潜在治疗方法.
科学领域:
- 环境健康 环境健康
- 内分泌学 在内分泌学.
- 骨生物学 骨生物学 骨生物学
背景情况:
- 双S (BPS) 被广泛使用,引发了环境和健康方面的担忧.
- 有限的研究存在于BPS对骨质稳定和骨质疏松的影响.
- 了解BPS对骨健康的影响对于公众健康至关重要.
研究的目的:
- 调查BPS暴露与骨矿物质密度 (BMD) 之间的关联.
- 阐明BPS诱导的骨损失背后的分子机制.
- 确定与BPS相关的骨质疏松症的潜在治疗干预措施.
主要方法:
- 分析国家健康和营养检查调查数据BPS-BMD相关性.
- 在体内小鼠模型暴露于与人类相当的BPS剂量6个月.
- 在体外研究中使用介质干细胞 (MSC) 与RNA-seq,分子对接和虚拟查.
主要成果:
- 在人类的尿路BPS水平和BMD之间发现了负相关性.
- 在小鼠中,BPS暴露导致股骨骨质量减少,表明骨质疏松症.
- BPS激活PPARγ,促进SMAD6的转录,抑制MSC的骨质分化.
- 在实验室中,Odanrigan有效地阻止了BPS-PPARγ相互作用,并逆转了BPS诱导的骨质疏松症.
结论:
- 在PPARγ-SMAD6信号通路中介于BPS诱导的骨质疏松症.
- 暴露于BPS对骨健康构成重大风险.
- 奥丹利根显示为治疗BPS诱导的骨质损失的治疗剂具有前途.
更多相关视频
08:43Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
11:38Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay
Published on: September 14, 2021
相关概念视频
TGF - β Signaling Pathway
Hormones and Bone Tissue
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Bone Remodeling
Osteoclasts in Bone Remodeling
The JAK-STAT Signaling Pathway