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Abstract：
BACKGROUND: Phlomis umbrosa Turczaninow root has been traditionally used to treat fractures, rheumatoid arthritis, and arthralgia. However, the effects and mechanisms of P. umbrosa on osteoarthritis (OA) remain poorly understood and a functional genomic approach has not been investigated.
OBJECTIVE: The purpose of this study was to investigate the effects and mechanisms of P. umbrosa extract (PUE) on OA using transcriptomic analysis.
METHODS: We performed joint diameter measurements, micro computed tomography, and histopathological analysis of monosodium iodoacetate (MIA)-induced OA rats treated with PUE (200 mg/kg) for 3 weeks. Gene expression profiling in articular cartilage tissue was then performed using RNA sequencing (RNA-seq) followed by signaling pathway analysis of regulatory genes.
RESULTS: PUE treatment improved OA based on decreased joint diameter, increased joint morphological parameters, and histopathological features. Many genes involved in multiple signal transduction pathway and collagen activation in OA were differentially regulated by PUE. These included genes related to Wnt/β-catenin, OA pathway, and sonic hedgehog signaling activity. Furthermore, PUE treatment downregulated cartilage damage factors (MMP-9, MMP-13, ADAMTs4, and ADMATs5) and upregulated chondrogenesis (COL2A1 and SOX-9) by regulating the transcription factors SOX-9, Ctnnb1, and Epas1.
CONCLUSIONS: Based on the results of gene expression profiling, this study highlighted the molecular mechanisms underlying the effects of PUE in MIA-induced OA rats. The findings provide novel insight into the mechanisms by which PUE treatment-induced gene expression changes may influence OA disease progression. Taken together, the results suggest that PUE may be used as a source of therapeutic agents for OA.
OBJECTIVE: The purpose of this study was to investigate the effects and mechanisms of P. umbrosa extract (PUE) on OA using transcriptomic analysis.
METHODS: We performed joint diameter measurements, micro computed tomography, and histopathological analysis of monosodium iodoacetate (MIA)-induced OA rats treated with PUE (200 mg/kg) for 3 weeks. Gene expression profiling in articular cartilage tissue was then performed using RNA sequencing (RNA-seq) followed by signaling pathway analysis of regulatory genes.
RESULTS: PUE treatment improved OA based on decreased joint diameter, increased joint morphological parameters, and histopathological features. Many genes involved in multiple signal transduction pathway and collagen activation in OA were differentially regulated by PUE. These included genes related to Wnt/β-catenin, OA pathway, and sonic hedgehog signaling activity. Furthermore, PUE treatment downregulated cartilage damage factors (MMP-9, MMP-13, ADAMTs4, and ADMATs5) and upregulated chondrogenesis (COL2A1 and SOX-9) by regulating the transcription factors SOX-9, Ctnnb1, and Epas1.
CONCLUSIONS: Based on the results of gene expression profiling, this study highlighted the molecular mechanisms underlying the effects of PUE in MIA-induced OA rats. The findings provide novel insight into the mechanisms by which PUE treatment-induced gene expression changes may influence OA disease progression. Taken together, the results suggest that PUE may be used as a source of therapeutic agents for OA.
摘要：
背景：树根传统上用于治疗骨折，类风湿性关节炎,和关节痛.然而,关于乌博沙对骨关节炎(OA)的作用和机制仍然知之甚少,也没有研究功能基因组方法.
目的：本研究的目的是通过转录组学分析来研究木薯提取物（PUE）对OA的影响和机制。
方法：我们进行了关节直径测量，微型计算机断层扫描，和碘乙酸钠（MIA）诱导的OA大鼠用PUE（200mg/kg）治疗3周的组织病理学分析。然后使用RNA测序(RNA-seq)进行关节软骨组织中的基因表达谱分析,随后进行调节基因的信号通路分析。
结果：PUE治疗基于减小的关节直径改善了OA，增加关节形态参数，和组织病理学特征。参与OA中多种信号转导通路和胶原活化的许多基因受到PUE的差异调控。这些包括与Wnt/β-catenin相关的基因，OA途径,和声波刺猬信号活动。此外，PUE治疗下调软骨损伤因子（MMP-9，MMP-13，ADAMTs4和ADMATs5），并通过调节转录因子SOX-9，Ctnnb1和Epas1上调软骨形成（COL2A1和SOX-9）。
结论：根据基因表达谱的结果，这项研究强调了PUE在MIA诱导的OA大鼠中作用的分子机制。这些发现为PUE治疗诱导的基因表达变化可能影响OA疾病进展的机制提供了新的见解。一起来看,结果表明,PUE可作为OA的治疗药物来源.
目的：本研究的目的是通过转录组学分析来研究木薯提取物（PUE）对OA的影响和机制。
方法：我们进行了关节直径测量，微型计算机断层扫描，和碘乙酸钠（MIA）诱导的OA大鼠用PUE（200mg/kg）治疗3周的组织病理学分析。然后使用RNA测序(RNA-seq)进行关节软骨组织中的基因表达谱分析,随后进行调节基因的信号通路分析。
结果：PUE治疗基于减小的关节直径改善了OA，增加关节形态参数，和组织病理学特征。参与OA中多种信号转导通路和胶原活化的许多基因受到PUE的差异调控。这些包括与Wnt/β-catenin相关的基因，OA途径,和声波刺猬信号活动。此外，PUE治疗下调软骨损伤因子（MMP-9，MMP-13，ADAMTs4和ADMATs5），并通过调节转录因子SOX-9，Ctnnb1和Epas1上调软骨形成（COL2A1和SOX-9）。
结论：根据基因表达谱的结果，这项研究强调了PUE在MIA诱导的OA大鼠中作用的分子机制。这些发现为PUE治疗诱导的基因表达变化可能影响OA疾病进展的机制提供了新的见解。一起来看,结果表明,PUE可作为OA的治疗药物来源.
