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梓醇通过增强内源性间充质干细胞的募集促进关节软骨修复。

Catalpol promotes articular cartilage repair by enhancing the recruitment of endogenous mesenchymal stem cells.

机构信息

Institute of Orthopaedics and Traumatology of Zhejiang Province, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.

The First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

J Cell Mol Med. 2024 Apr;28(7):e18242. doi: 10.1111/jcmm.18242.

DOI:10.1111/jcmm.18242
PMID:38509736
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10955160/
Abstract

Articular cartilage defect is challenged by insufficient regenerative ability of cartilage. Catalpol (CA), the primary active component of Rehmanniae Radix, could exert protective effects against various diseases. However, the impact of CA on the treatment of articular cartilage injuries is still unclear. In this study, full-thickness articular cartilage defect was induced in a mouse model via surgery. The animals were intraperitoneally injected with CA for 4 or 8 weeks. According to the results of macroscopic observation, micro-computed tomography CT (μCT), histological and immunohistochemistry staining, CA treatment could promote mouse cartilage repair, resulting in cartilage regeneration, bone structure improvement and matrix anabolism. Specifically, an increase in the expression of CD90, the marker of mesenchymal stem cells (MSCs), in the cartilage was observed. In addition, we evaluated the migratory and chondrogenic effects of CA on MSCs. Different concentration of CA was added to C3H10 T1/2 cells. The results showed that CA enhanced cell migration and chondrogenesis without affecting proliferation. Collectively, our findings indicate that CA may be effective for the treatment of cartilage defects via stimulation of endogenous MSCs.

摘要

关节软骨缺损是由软骨再生能力不足引起的。梓醇(CA)是地黄的主要活性成分,对多种疾病具有保护作用。然而,CA 对关节软骨损伤的治疗作用尚不清楚。本研究通过手术在小鼠模型中诱导全层关节软骨缺损。动物经腹腔注射 CA 4 或 8 周。根据宏观观察、微计算机断层扫描(μCT)、组织学和免疫组织化学染色的结果,CA 治疗可促进小鼠软骨修复,从而促进软骨再生、改善骨结构和基质合成代谢。具体而言,观察到软骨中间充质干细胞(MSCs)标志物 CD90 的表达增加。此外,我们评估了 CA 对 MSCs 的迁移和软骨生成作用。将不同浓度的 CA 添加到 C3H10T1/2 细胞中。结果表明,CA 增强了细胞迁移和软骨生成,而不影响增殖。总之,我们的研究结果表明,CA 可能通过刺激内源性 MSCs 对软骨缺损的治疗有效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/83757b5f17b4/JCMM-28-e18242-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/34826afecc8a/JCMM-28-e18242-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/62e3c373501b/JCMM-28-e18242-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/a065a6c97886/JCMM-28-e18242-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/c21bf27d42ad/JCMM-28-e18242-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/15c9dece92f2/JCMM-28-e18242-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/83757b5f17b4/JCMM-28-e18242-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/34826afecc8a/JCMM-28-e18242-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/62e3c373501b/JCMM-28-e18242-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/a065a6c97886/JCMM-28-e18242-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/c21bf27d42ad/JCMM-28-e18242-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/15c9dece92f2/JCMM-28-e18242-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a3d/10955160/83757b5f17b4/JCMM-28-e18242-g006.jpg

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