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Background <p>The incidence of knee osteoarthritis (KOA) continues to rise with the aging of the population, which seriously reduces the quality of life of patients. Platelet-rich plasma (PRP), a biological agent rich in growth factors and cytokines, has shown promising potential in the treatment of KOA in recent years. However, the specific molecular mechanism of its regulation of the pathological process is not clear.</p> Methods <p>Based on the GSE157364 dataset, DESeq2 software was used to analyze the differentially expressed genes (DEGs) of OA-FLSs between the PRP group and the Ctrl group. KEGG pathway and GO function enrichment analysis were performed by SangerBox. The genes related to cell senescence, inflammatory response and oxidative stress were screened from the GeneCards database, and the intersection was obtained by a Venn diagram.</p> Results <p>911 DEGs (398 upregulated and 513 downregulated) were screened out. The expression of the key gene <i>UBE2C</i> in OA-FLSs was significantly downregulated compared with that in N-FLSs. PRP treatment significantly upregulated UBE2C expression in OA-FLSs, inhibited pro-inflammatory cytokine secretion, reduced intracellular ROS levels and β-Gal-positive senescent cell numbers, restored mitochondrial membrane potential, and downregulated the senescence-related proteins P21, P16, and P53.</p> Conclusion <p>PRP can inhibit the inflammatory response, oxidative stress injury, and cell senescence of OA-FLSs by upregulating the expression of <i>UBE2C</i>, thereby delaying the pathological process of KOA, which provides a new molecular target and theoretical basis for the clinical treatment of KOA.</p> Graphical Abstract <p></p>

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Mechanism of platelet-rich plasma inhibiting inflammatory response, oxidative stress, and senescence in synovial fibroblasts of patients with knee osteoarthritis via UBE2C based on transcriptome sequencing analysis

  • 期刊论文

  • 发表日期：

    2026年3月26日

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  • Lili Zou,
  • Yujuan Ma,
  • Mingxian Hu,
  • Zhenshuang Sun,
  • Zhijun Shi,
  • Jiahuan Gao,
  • Xiguo Cai

摘要

Background

The incidence of knee osteoarthritis (KOA) continues to rise with the aging of the population, which seriously reduces the quality of life of patients. Platelet-rich plasma (PRP), a biological agent rich in growth factors and cytokines, has shown promising potential in the treatment of KOA in recent years. However, the specific molecular mechanism of its regulation of the pathological process is not clear.

Methods

Based on the GSE157364 dataset, DESeq2 software was used to analyze the differentially expressed genes (DEGs) of OA-FLSs between the PRP group and the Ctrl group. KEGG pathway and GO function enrichment analysis were performed by SangerBox. The genes related to cell senescence, inflammatory response and oxidative stress were screened from the GeneCards database, and the intersection was obtained by a Venn diagram.

Results

911 DEGs (398 upregulated and 513 downregulated) were screened out. The expression of the key gene UBE2C in OA-FLSs was significantly downregulated compared with that in N-FLSs. PRP treatment significantly upregulated UBE2C expression in OA-FLSs, inhibited pro-inflammatory cytokine secretion, reduced intracellular ROS levels and β-Gal-positive senescent cell numbers, restored mitochondrial membrane potential, and downregulated the senescence-related proteins P21, P16, and P53.

Conclusion

PRP can inhibit the inflammatory response, oxidative stress injury, and cell senescence of OA-FLSs by upregulating the expression of UBE2C, thereby delaying the pathological process of KOA, which provides a new molecular target and theoretical basis for the clinical treatment of KOA.

Graphical Abstract