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| 脂联素改善炎症微环境抑制骨吸收治疗糖尿病性骨质疏松 |
| Adiponectin improves inflammatory microenvironment to inhibit bone resorption for the treatment of diabetic osteoporosis |
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| DOI：10.3969/j.issn.1006-7108.2025.05.007 |
| 中文关键词: 脂联素 炎症环境 骨吸收 糖尿病性骨质疏松 |
| 英文关键词:adiponectin inflammatory bone resorption diabetic osteoporosis |
| 基金项目:新疆维吾尔自治区自然科学基金面上项目(2022D01C542) |
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| 中文摘要: |
| 目的 探究外源性脂联素对糖尿病相关骨质疏松症的治疗效果，评估其对破骨细胞形成和骨微细结构的影响。方法 构建糖尿病模型小鼠，将其随机分为对照组、糖尿病模型组和脂联素治疗组。使用酶联免疫吸附测定(ELISA)检测循环脂联素和炎症因子水平，采用实时荧光定量PCR分析破骨细胞分化标志基因，使用骨组织学技术评估骨微细结构。结果 糖尿病模型小鼠的循环脂联素浓度显著降低(P＜0.0001)，脂联素治疗组的循环脂联素水平明显上升(P＜0.0001)。与对照组相比，糖尿病模型小鼠的TNF-α、IL-6 和 IFNγ水平显著升高(P＜0.0001)。脂联素治疗后，炎症因子水平显著降低(P＜0.0001)。糖尿病模型小鼠的破骨细胞数量增多，破骨分化标志基因显著上调。脂联素治疗后，成熟破骨细胞数量显著减少(P＜0.0001)，破骨分化标志基因Ctsk、Nfatc1明显降低(P＜0.0001)。与对照组相比，糖尿病模型小鼠的骨小梁面积和厚度显著减少(P＜0.0001)。脂联素治疗组的骨小梁面积和厚度部分恢复(P＜0.0001)，但仍低于对照组。结论 补充外源性脂联素可以显著抑制糖尿病相关的破骨细胞形成，部分恢复骨小梁面积和厚度，改善糖尿病引起的骨丢失。潜在机制可能是通过改善炎症微环境抑制骨吸收。 |
| 英文摘要: |
| Objective To investigate the therapeutic effect of exogenous adiponectin on diabetic osteoporosis and evaluate its impact on osteoclast formation and bone microstructure. Methods Diabetic model mice were constructed and randomly divided into control group, diabetic model group, and adiponectin treatment group. The levels of circulating adiponectin and inflammatory factors were measured using enzyme-linked immunosorbent assay (ELISA). Real-time quantitative PCR was employed to analyze osteoclast differentiation marker genes, while bone histological techniques were used to assess bone microstructure. Results The circulating adiponectin level in diabetic model mice was significantly lower (P<0.0001), while the adiponectin level in the treatment group showed a significant increase (P<0.0001). Compared with the control group, the levels of TNF-α, IL-6, and IFNγ were significantly elevated in the diabetic model group (P<0.0001). After adiponectin treatment, the levels of inflammatory factors significantly decreased (P<0.0001). The number of osteoclasts in the diabetic model mice increased, with elevated levels of osteoclast differentiation marker genes. However, the number of mature osteoclasts in the adiponectin treatment group significantly decreased (P<0.0001), with significant reductions in Ctsk and Nfatc1 expression (P<0.0001). The bone trabecular area and thickness were significantly reduced in the diabetic model group compared with the control group (P<0.0001). The adiponectin treatment group showed partial recovery in bone trabecular area and thickness (P<0.0001), although they remained lower than in the control group. Conclusion Supplementation with exogenous adiponectin significantly inhibits osteoclast formation related to diabetes, partially restores bone trabecular area and thickness, and mitigates bone loss caused by diabetes. The potential mechanism may involve improved inflammatory microenvironment leading to reduced bone resorption. |
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