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慢性神经源性疼痛由于其发病机制尚不完全明确,目前还没有十分有效的治疗手段;神经损伤后炎症反应和免疫调节机制在疼痛的发生中发挥着重要作用,透明质酸(HA)近来被认为是炎症和免疫调节中一个重要的调节分子。为了进一步研究HA是否参与到神经损伤后的病理过程中,我们检测了慢性压迫性神经损伤(CC I)大鼠损伤神经的HA含量。结果显示:与正常神经比较,HA的含量在损伤后7 d明显增加,HA合成酶(HAS)的表达也明显上调。4-甲基伞形酮(4-MU)是HAS的一种抑制剂,我们通过给予4-MU抑制HA的合成,研究HA在慢性神经源性疼痛中的作用,发现给药组CC I大鼠损伤足对热痛刺激的敏感性低于未给药组,同时IL-1β的表达量低于未给药组。以上结果提示HA可能通过对炎症因子的调控参与到损伤后的疼痛机制中,这一结果将有助于慢性神经源性疼痛的治疗。
Chronic neuropathic pain is not yet completely effective because its pathogenesis is not yet fully understood. Inflammatory and immunoregulatory mechanisms play an important role in the development of pain after nerve injury. Hyaluronic acid (HA) has recently been It is thought to be an important regulator of inflammation and immune regulation. To further investigate whether HA participates in pathological processes after nerve injury, we examined the HA content of the injured nerves in chronic compression nerve injury (CCI) rats. The results showed that compared with normal nerves, the content of HA significantly increased at 7 d and the expression of HA synthase (HAS) was also significantly up-regulated. 4-Methylumbelliferone (4-MU) is an inhibitor of HAS. We investigated the effect of HA on chronic neuropathic pain by inhibiting the synthesis of HA by administering 4-MU and found that the CCI large The sensitivity of the injured foot to heat pain was lower than that of the untreated group, while the expression of IL-1β was lower than that of the untreated group. These results suggest that HA may participate in the post-injury pain mechanism through the regulation of inflammatory cytokines, and this result will be helpful for the treatment of chronic neurogenic pain.