在雄性大鼠中,迪戈辛通过RORγt依赖的Th17反应减弱了与双酸盐相关的骨缩
相关实验视频
Updated: Jun 12, 2025

08:56
Estrogen-Like Effect of Bazi Bushen Capsule in Ovariectomized Rats
Published on: April 7, 2023
841
José Vitor Mota Lemos1, Joyce Ohana de Lima Martins1, Larissa Carvalho Machado2
1Department of Clinical Dentistry, Division of Oral Pathology, School of Pharmacy, Dentistry and Nursing, Universidade Federal do Ceará, Fortaleza, Ceará, Brazil.
Oral surgery, oral medicine, oral pathology and oral radiology
|September 20, 2024
概括
在大鼠中,迪戈辛治疗显著减少了与药物相关的骨缩 (MRONJ),通过抑制RORγt和Th17免疫反应. 这为MRONJ提供了潜在的治疗途径.
科学领域:
- 口腔和牙面部外科手术
- 药理学 药理学是指药理学的学科.
- 免疫学 免疫学 免疫学
背景情况:
- 与药物相关的骨缩 (MRONJ) 是一种严重的并发症,与抗吸收药物,如龙酸 (ZA) 相关.
- 与视网膜酸受体相关的孤儿受体马t (RORγt) 和T助手17 (Th17) 途径在MRONJ病原发生中的作用越来越被认可.
研究的目的:
- 为了研究已知RORγt抑制剂迪戈辛的治疗潜力,在鼠标模型中研究了勒龙酸诱导的MRONJ.
- 评估狄戈辛对关键病理标志物和与MRONJ相关的免疫反应的影响.
主要方法:
- 雄性Wistar大鼠被给予佐列龙酸 (ZA) 来诱导MRONJ,然后用不同剂量的迪戈辛治疗.
- 部组织使用放射,组织形态测量和免疫组织化学方法进行了分析.
- 牙组织通过西式涂抹进行评估,并测试大腿骨的机械性质.
主要成果:
- 迪戈辛治疗显著降低了MRONJ相关的放射性,炎症细胞透和骨细胞亡.
- 迪戈辛抑制了关键的炎症标志物,包括介质蛋白-17 (IL-17),TNF-α和IL-6,并逆转了RORγt表达.
- 虽然增加了腹和器官指数,但狄戈辛也增强了股骨的机械强度.
结论:
- 在大鼠模型中,迪戈辛有效地减弱了MRONJ,主要是通过抑制RORγt和降低Th17免疫反应.
- 这些发现表明,用狄戈辛准RORγt可能代表一种用于管理MRONJ的新型治疗策略.
相关概念视频
Hormones and Bone Tissue
2.6K
The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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...
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...
2.6K
Osteoclasts in Bone Remodeling
2.8K
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
2.8K
Bone Disorders
3.4K
Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
3.4K
Bone Remodeling
38.2K
Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
38.2K

