Transcriptomic insights into the anti-apoptotic effect of Tuina in rabbit model of intervertebral disc degeneration

推拿在兔椎间盘退变模型中抗凋亡作用的转录组学研究

阅读:1

Abstract

BACKGROUND: Tuina therapy is a promising treatment for spinal diseases, but its therapeutic mechanism remains poorly understood. Nucleus pulposus (NP) cell apoptosis is an important pathologic mechanism of intervertebral disc degeneration (IDD). We evaluated the intervention effect of sham-controlled placebo therapy on NP apoptosis in rabbit model of IDD and dissected the molecular mechanism by transcriptome analysis. METHODS: IDD rabbit model was established by using intervertebral disc fibrous annulus puncture, and the intervention was carried out for 4 weeks in the Tuina group and the Placebo group. The intervention effects of the two therapies were assessed by H&E staining, MRI scanning, Tunel staining and flow cytometry. Transcriptome analysis was performed to detect key differentially expressed genes (DEGs) and related signaling pathways. The mRNA expression levels of key differentially expressed genes were verified by RT-qPCR. RESULTS: Compared with the Placebo therapy, the Tuina intervention was superior in inhibiting nucleus pulposus cell apoptosis and maintenance of disc morphology and structure. Protein-Protein Interaction (PPI) analysis showed that there were common differentially expressed genes among the Tuina, Placebo and Model groups. The mRNA expression of core signaling factors RPL17, LOC100354980 and LOC100339314 was consistent with the transcriptome sequencing results after the Tuina intervention, as verified by RT-qPCR. CONCLUSION: Our results suggest that compared to Placebo therapy, Tuina intervention showed improved effects on tissue structural morphology and NP cell apoptosis. Tuina slowed down NP cell apoptosis in the rabbit model of IDD, which may be related to pathways such as Wnt, and the RPL17 gene may be a promising therapeutic target, and further studies are needed to elucidate their functional profile in IDD.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。