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Aim <p>To investigate the activity of Ras-related C3 botulinum toxin substrate 1(Rac1) in the lumbar facet joint osteoarthritis(FJOA).</p> Methods <p>Fifty-five lumbar facet joint samples were collected from clinical patients, and they were divided into three groups according to Weishaup classification. Hematoxylin-eosin staining, Safranin O/Fast green staining, and the OARSI scoring system were used to assess the severity of cartilage degeneration. The activity of Rac1 was detected by pull-down assay.A rat lumbar FJOA model was constructed using sodium iodoacetate. Immunohistochemical staining was used to detect the expression of COL2 and MMP13 in rat cartilage tissue. SW1353 cells were stimulated with IL-1β to construct a model of chondrocyte apoptosis.The expression of COL2,MMP13, NF-κB signaling pathway proteins and apoptosis proteins were detected by western blotting. Immunofluorescence was used to detect the expression changes and co-localization of Rac1, COL2, and MMP13.NSC23766 was used to inhibit the activation of Rac1. TUNEL assay was used to detect the effect of chondrocyte apoptosis.</p> Results <p> The activity of Rac1 was increased in the cartilage tissue of the lumbar facet joint in osteoarthritis.IL-1β induced an increase of Rac1 activity in SW1353 cells, and promoted chondrocyte apoptosis through the NF-κB signaling pathway.NSC23766 inhibited the increase of Rac1 activity induced by IL-1β, and reduced chondrocyte apoptosis by inhibiting the NF-ΚB signaling pathway.</p> Conclusions <p> The activity of Rac1 is increased in the cartilage tissue of lumbar FJOA, and the increase of activity of Rac1 induced by IL-1β can participates in the apoptosis of chondrocytes through the NF-κB signaling pathway.</p>

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Activated Rac1 promotes chondrocyte apoptosis through the NF-κB pathway in lumbar facet joint osteoarthritis

  • 期刊论文

  • 发表日期：

    2026年2月25日

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  • Xiangyu Wang,
  • Pengfei Xue,
  • Jinlong Zhang,
  • Huricha Jin,
  • Jiawei Jiang,
  • Guanhua Xu,
  • Zhiming Cui

摘要

Aim

To investigate the activity of Ras-related C3 botulinum toxin substrate 1(Rac1) in the lumbar facet joint osteoarthritis(FJOA).

Methods

Fifty-five lumbar facet joint samples were collected from clinical patients, and they were divided into three groups according to Weishaup classification. Hematoxylin-eosin staining, Safranin O/Fast green staining, and the OARSI scoring system were used to assess the severity of cartilage degeneration. The activity of Rac1 was detected by pull-down assay.A rat lumbar FJOA model was constructed using sodium iodoacetate. Immunohistochemical staining was used to detect the expression of COL2 and MMP13 in rat cartilage tissue. SW1353 cells were stimulated with IL-1β to construct a model of chondrocyte apoptosis.The expression of COL2,MMP13, NF-κB signaling pathway proteins and apoptosis proteins were detected by western blotting. Immunofluorescence was used to detect the expression changes and co-localization of Rac1, COL2, and MMP13.NSC23766 was used to inhibit the activation of Rac1. TUNEL assay was used to detect the effect of chondrocyte apoptosis.

Results

The activity of Rac1 was increased in the cartilage tissue of the lumbar facet joint in osteoarthritis.IL-1β induced an increase of Rac1 activity in SW1353 cells, and promoted chondrocyte apoptosis through the NF-κB signaling pathway.NSC23766 inhibited the increase of Rac1 activity induced by IL-1β, and reduced chondrocyte apoptosis by inhibiting the NF-ΚB signaling pathway.

Conclusions

The activity of Rac1 is increased in the cartilage tissue of lumbar FJOA, and the increase of activity of Rac1 induced by IL-1β can participates in the apoptosis of chondrocytes through the NF-κB signaling pathway.