Contralateral monoarthritis exacerbated chronic constriction injury-induced pain hypersensitivity through upregulating inducible nitric oxide synthase

对侧单关节炎通过上调诱导型一氧化氮合酶加剧慢性压迫性损伤引起的疼痛过敏

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作者:Heng Zhao, Shenghou Liu, Chenhua Wang, Qingjie Wang, Wenguang Liu, Mingzhi Gong

Conclusion

Inhibiting the iNOS might be a potential therapeutic strategy for concurrent OA and neuropathic pain.

Discussion

Interestingly, intrathecal injection of 1400W, an antagonist of iNOS, attenuated intensity of pain behaviors in CCI rats with contralateral MA to similar levels in CCI rats without MA, and also normalized the facilitatory effect of forskolin on excitatory synaptic transmission in the spinal cord dorsal horn neurons in contralateral MA rats. Therefore, contralateral MA worsened CCI-induced pain hypersensitivity probably through upregulating iNOS and enhancing the facilitation of synaptic transmission following CCI. Conclusion: Inhibiting the iNOS might be a potential therapeutic strategy for concurrent OA and neuropathic pain.

Methods

To address whether neuropathic pain is affected by contralateral MA through distinct inflammatory pathway, MA was induced by intra-articular injection of complete Freund's adjuvant (CFA) into the right tibiotarsal joint, and neuropathic pain was established by chronic constriction injury (CCI) of the left sciatic nerve.

Results

We observed that MA aggravated mechanical allodynia and thermal hyperalgesia in CCI rats. Furthermore, MA affected the other side of the spinal cord in multiple aspects, including the upregulation of iNOS mRNA and the enhancement of forskolin-induced facilitation of excitatory synaptic transmission in the spinal cord dorsal horn substantia gelatinosa neurons.

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