| 凌厚福.肾髓同治方对小鼠膝骨关节炎模型的干预机制研究[J].浙江中西医结合杂志,2024,34(8): |
| 肾髓同治方对小鼠膝骨关节炎模型的干预机制研究 |
| Study on the intervention mechanism of Shensui Tongzhi Formula on a mouse model of knee osteoarthritis |
| 投稿时间：2023-11-27 修订日期：2024-08-04 |
| DOI： |
| 中文关键词: 骨关节炎、肾髓同治方、软骨细胞、TGF-β/Smad信号通路 |
| 英文关键词:Osteoarthritis, Shensui Tongzhi Formula, Chondrocytes, TGF-β/Smad signaling pathway |
| 基金项目:国家自然科学基金资助项目(No. 82305266), |
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| 中文摘要: |
| 目的 探讨肾髓同治方对小鼠膝骨关节炎的疗效的分子机制 方法 24只雄性C57BL/6J小鼠,随机分为假手术组、模型组、肾髓同治方低剂量组和肾髓同治方高剂量组,每组6只。模型组、肾髓同治方低剂量组和肾髓同治方高剂量组通过内侧半月板失稳术(destabilization of the medial meniscus, DMM)以构建 OA模型。灌胃8周后,Micro-CT观察胫骨侧软骨下骨骨微结构,番红固绿染色观察组织病理变化,免疫组织化学检测Col2、Mmp13和pSmad2的变化。结果: 与假手术组相比,模型组小鼠软骨下骨骨小梁厚度和骨小梁数量显著增加,同时骨小梁分离度显著减小；番红固绿病理染色发现关节软骨严重磨损,软骨厚度及面积减少,剩余软骨细胞多数呈肥大状态,软骨下骨硬化明显；免疫组织化学发现胫骨侧关节软骨的Col2及pSmad2表达水平明显下降,Mmp13表达水平显著上升。与模型组相比,肾髓同治方低剂量组和肾髓同治方高剂量可以有效的改善软骨下骨硬化的情况,表现为骨小梁厚度和骨小梁数量显著降低及骨小梁分离度的显著增高；且关节软骨磨损明显减轻,软骨厚度得到保留,且软骨下骨硬化得到显著改善；Col2及pSmad2蛋白的表达水平显著提高,同时Mmp13的表达水平被抑制。结论 肾髓同治方对小鼠膝骨关节炎有一定的防治作用,其主要机制与调控软骨细胞的TGF-β/Smad信号通路有关。 |
| 英文摘要: |
| Objective: To explore the molecular mechanism of the efficacy of Shensui Tongzhi Formula (SSTZF) on osteoarthritis of the knee in mice Methods: Twenty-four male C57BL/6J mice were randomly divided into sham-operated group, model group, SSTZF low-dose group and SSTZF high-dose group, six mice in each group. The model group, the SSTZF low-dose group and the SSTZF high-dose group underwent destabilization of the medial meniscus (DMM) to construct the OA model. After 8 weeks of gavage, Micro-CT was used to observe the bone microstructure of the lateral subchondral bone of the tibia, and the histopathological changes were observed by Senna solid green staining, and the changes of Col2, Mmp13 and pSmad2 were detected by immunohistochemistry. Results: Compared with the sham-operated group, the thickness and number of trabeculae of the subchondral bone in the model group were significantly increased, and the separation of trabeculae was significantly reduced; the pathological staining of sapphire green revealed that the articular cartilage was severely abraded, with the thickness and area of the cartilage reduced, most of the remaining chondrocytes in the cartilage were in the state of hypertrophy, and the sclerosis of the subchondral bone was obvious; immunohistochemistry revealed that the expression level of Col2 and pSmad2 of the tibial side articular cartilage was significantly decreased, and the expression level of Mmp13 was significantly decreased. Immunohistochemistry showed that the expression levels of Col2 and pSmad2 in the articular cartilage of the tibial side were significantly decreased, and the expression level of Mmp13 was significantly increased. Compared with the model group, the SSTZF low-dose group and the SSTZF high-dose group could effectively improve the subchondral osteosclerosis, which was manifested by the significant reduction of trabecular thickness and number of trabeculae, and the significant increase of trabecular separation; and the articular cartilage abrasion was significantly reduced, and the thickness of the cartilage was preserved, and the subchondral osteosclerosis was significantly improved; and the expression levels of Col2 and pSmad2 proteins were significantly increased, and the expression levels of Mmp13 were significantly increased, while the expression level of Mmp13 was suppressed. Conclusions: SSTZF has a certain preventive effect on osteoarthritis of the knee in mice, and its main mechanism is related to the TGF-β/Smad signaling pathway that regulates chondrocytes. |
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