Osteoking 通过调节 AGEs/IGF-1/β-catenin/OPG 通路,防止 2 型糖尿病 db/db 小鼠骨质流失并促进成骨细胞骨形成。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Yi Yang, Rong Li, Peijin Wang, Yulan Zhao, Jintao Li, Jianlin Jiao, Hong Zheng
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引用次数: 0

摘要

2 型糖尿病骨质疏松症(T2DOP)是一种骨骼代谢综合征,其特征是由 2 型糖尿病导致的骨重塑受损,目前的治疗方法存在缺陷。Osteoking(OK)被广泛用于治疗骨折和股骨头坏死。然而,OK 在 T2DOP 领域鲜有报道,其作用和作用机制也有待阐明。因此,本研究探讨了 OK 是否能改善骨重塑以及糖尿病诱导损伤的机制。我们以 db/db 小鼠为 T2DOP 模型,分别用高糖(HG,50 mM)和高级糖化终产物(AGEs,100 µg/mL)刺激 MC3T3-E1 细胞(成骨细胞系)。采用三点机械弯曲试验、苏木精和伊红染色以及酶联免疫吸附试验综合评估了 OK 对 T2DOP 的影响。碱性磷酸酶活性测定和茜素红 S 染色法评估了 OK 在 HG 和 AGEs 条件下增强 MC3T3-E1 细胞分化和矿化的效果。AGEs/胰岛素样生长因子-1(IGF-1)/β-catenin/osteoprotegerin(OPG)通路相关蛋白水平通过Western印迹分析和免疫组化染色进行了检测。我们发现,OK能降低db/db小鼠的高血糖,减轻骨损伤,修复骨重塑,增加胫骨和股骨IGF-1、β-catenin和OPG的表达,降低核卡巴B受体激活剂配体和核卡巴B受体激活剂的表达。此外,OK还能分别促进HG和AGEs条件下MC3T3-E1细胞的分化和矿化,并调节AGEs/IGF-1/β-catenin/OPG通路相关蛋白的水平。总之,我们的研究结果表明,OK 可通过激活 AGEs/IGF-1/β-catenin/OPG 通路降低血糖、减轻骨损伤并减轻 T2DOP。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Osteoking prevents bone loss and enhances osteoblastic bone formation by modulating the AGEs/IGF-1/β-catenin/OPG pathway in type 2 diabetic db/db mice

Type 2 diabetic osteoporosis (T2DOP) is a skeletal metabolic syndrome characterized by impaired bone remodeling due to type 2 diabetes mellitus, and there are drawbacks in the present treatment. Osteoking (OK) is widely used for treating fractures and femoral head necrosis. However, OK is seldom reported in the field of T2DOP, and its role and mechanism of action need to be elucidated. Consequently, this study investigated whether OK improves bone remodeling and the mechanisms of diabetes-induced injury. We used db/db mice as a T2DOP model and stimulated MC3T3-E1 cells (osteoblast cell line) with high glucose (HG, 50 mM) and advanced glycation end products (AGEs, 100 µg/mL), respectively. The effect of OK on T2DOP was assessed using a combined 3-point mechanical bending test, hematoxylin and eosin staining, and enzyme-linked immunosorbent assay. The effect of OK on enhancing MC3T3-E1 cell differentiation and mineralization under HG and AGEs conditions was assessed by an alkaline phosphatase activity assay and alizarin red S staining. The AGEs/insulin-like growth factor-1(IGF-1)/β-catenin/osteoprotegerin (OPG) pathway-associated protein levels were assayed by western blot analysis and immunohistochemical staining. We found that OK reduced hyperglycemia, attenuated bone damage, repaired bone remodeling, increased tibial and femoral IGF-1, β-catenin, and OPG expression, and decreased receptor activator of nuclear kappa B ligand and receptor activator of nuclear kappa B expression in db/db mice. Moreover, OK promoted the differentiation and mineralization of MC3T3-E1 cells under HG and AGEs conditions, respectively, and regulated the levels of AGEs/IGF-1/β-catenin/OPG pathway-associated proteins. In conclusion, our results suggest that OK may lower blood glucose, alleviate bone damage, and attenuate T2DOP, in part through activation of the AGEs/IGF-1/β-catenin/OPG pathway.

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来源期刊
Cell Biology International
Cell Biology International 生物-细胞生物学
CiteScore
7.60
自引率
0.00%
发文量
208
审稿时长
1 months
期刊介绍: Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.
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