首页> 外文期刊>International journal of molecular medicine >Transplantation of allogenic nucleus pulposus cells attenuates intervertebral disc degeneration by inhibiting apoptosis and increasing migration
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Transplantation of allogenic nucleus pulposus cells attenuates intervertebral disc degeneration by inhibiting apoptosis and increasing migration

机译:通过抑制细胞凋亡和增加迁移,发生同种异体髓核细胞的移植衰减椎间盘变性

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摘要

Transplantation of nucleus pulposus cells (NPCs) into the intervertebral disc (IVD) has been demonstrated to be an effective treatment of degenerative disc disease (DDD). However, the underlying mechanisms have remained to be sufficiently elucidated. The aim of the present study was to explore the potential cell migration and anti-apoptosis efficacy of NPCs in the treatment of DDD. NPCs cultured from rats expressing green fluorescent protein (GFP-NPCs) were transplanted into the degenerated IVD, and the migration of GFP-NPCs, as well as the degeneration and apoptosis of the IVD were detected to evaluate the therapeutic effect in vivo. In vitro, disc chondrocytes (DCs) and annulus fibrosus cells (AFCs) were co-cultured to explore the underlying mechanism. The results demonstrated that injection of NPCs suppressed DDD by inhibiting apoptosis and increasing extracellular matrix in vivo and in vitro. NPCs migrated into the inner AF in vivo, and NPC migration was observed to be promoted by AFCs and DCs in vitro, particularly by damaged AFCs. These results demonstrated the anti-apoptotic effects and migratory capacity of allogenic NPCs transplanted into the IVD, which evidences the contribution of NPCs to disc regeneration and provide a novel strategy for treating DDD.
机译:已经证明了核髓细胞(NPC)进入椎间盘(IVD)的移植是对退行性椎间盘疾病(DDD)的有效治疗方法。然而,潜在的机制仍然足够阐明。本研究的目的是探讨NPC在DDD治疗中NPC的潜在细胞迁移和抗凋亡疗效。将从表达绿色荧光蛋白(GFP-NPC)的大鼠培养的NPC移植到退化的IVD中,并检测到IVD的GFP-NPC的迁移,以及IVD的退化和凋亡,以评估体内的治疗效果。体外,椎间盘软骨细胞(DCS)和环状纤维细胞(AFC)共培养以探索下面的机制。结果表明,通过抑制细胞凋亡和增加体内和体外的细胞外基质来注射NPCs抑制DDD。将NPC迁移到体内内部AF中,并且观察到NPC迁移,以AFCS和DCS在体外促进,特别是通过受损的AFC。这些结果证明了移植到IVD中的同种异体NPC的抗凋亡效应和迁移能力,这证明了NPC对椎间盘再生的贡献,并提供了一种治疗DDD的新策略。

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