Department of Medical Cell Biology and Genetics, Guangdong Key Laboratory of Genomic Stability and Disease Prevention, Shenzhen Key Laboratory of Anti-aging and Regenerative Medicine, and Shenzhen Engineering Laboratory of Orthopaedic Regenerative Technologies, Health Sciences Center, Shenzhen University, Shenzhen, 518060, China.
Shenzhen Alps Cell Technologies Ltd, Longhua District, Shenzhen, Guangdong Province, China.
Biol Trace Elem Res. 2020 Feb;193(2):422-433. doi: 10.1007/s12011-019-01711-9. Epub 2019 May 3.
Osteoarthritis (OA), a common degenerative disease affecting articular cartilage, is caused by multiple factors, and currently, there are few approaches to effectively delay its progression. This study aimed to evaluate whether a strontium compound (in the form of strontium gluconate, Glu-Sr) could reduce OA pathology severity in osteoarthritic rat models by directly targeting chondrocytes, including catabolic/anabolic activities and/or chondrogenic differentiation. Glu-Sr was administered to OA rats by oral gavage beginning during OA induction and continuing for 8 weeks. Glu-Sr treatment was found to significantly reduce cartilage degeneration and delay OA progression. Further examination showed that collagen II, Sox9, and aggrecan (ACAN) genes were up-regulated whereas IL-1β was down-regulated in chondrocytes isolated from Glu-Sr-treated rats. Glu-Sr also antagonized the catabolic effects of IL-1β on chondrocytes. Furthermore, Glu-Sr was shown to promote the chondrogenic differentiation of bone marrow mesenchymal stem cells (BMMSCs), possibly through promoting chondrogenic gene expression, including CTGF and FGF1, as revealed by RNA-sequencing (RNA-seq). These results suggest that systemic administration of Glu-Sr may be useful in prophylactic and therapeutic treatment of chronic cartilage degradation through affecting multiple steps from chondrogenic differentiation of progenitors to matrix formation in mature chondrocytes.
骨关节炎(OA)是一种常见的关节软骨退行性疾病,由多种因素引起,目前很少有方法能有效延缓其进展。本研究旨在评估一种锶化合物(葡萄糖酸锶形式,Glu-Sr)是否可以通过直接靶向软骨细胞,包括分解代谢/合成代谢活性和/或软骨分化,来减轻骨关节炎大鼠模型中的 OA 病理严重程度。在 OA 诱导期间开始通过口服灌胃向 OA 大鼠给予 Glu-Sr,并持续 8 周。结果发现,Glu-Sr 治疗可显著减轻软骨退变并延缓 OA 进展。进一步的检查表明,在 Glu-Sr 处理的大鼠的软骨细胞中,胶原 II、Sox9 和聚集蛋白聚糖(ACAN)基因上调,而白细胞介素 1β(IL-1β)下调。Glu-Sr 还拮抗了 IL-1β对软骨细胞的分解代谢作用。此外,Glu-Sr 被证明可以通过促进 CTGF 和 FGF1 等软骨形成基因的表达来促进骨髓间充质干细胞(BMMSCs)的软骨分化,这一点通过 RNA 测序(RNA-seq)得到了证实。这些结果表明,系统给予 Glu-Sr 可能通过影响从祖细胞的软骨分化到成熟软骨细胞的基质形成的多个步骤,对慢性软骨降解的预防和治疗有用。