There is no effective treatment for peripheral nerve injury-induced chronic neuropathic pain (NP), which profoundly impacts the quality of life of those affected. Transmembraneprotein100 (TMEM100) is considered to be a pain regulatory protein and is expressed in the dorsal root ganglion (DRG) of rats. However, the mechanism of pain regulation and the expression of TMEM100 following various peripheral nerve injuries are unclear. In this study, we constructed two pain models of peripheral nerve injury: tibial nerve injury (TNI) and chronic constriction injury (CCI). This study found that the Paw Withdrawal Mechanical Threshold (PWMT) and Paw Withdraw Thermal Latency (PWTL) of the rats in the two pain models decreased significantly, and the expression of TMEM100 in the DRG of two groups also decreased significantly. Furthermore, the decrease in the CCI group was more obvious than in the TNI group. There was no significant statistical significance (). We constructed an adeno-associated virus 6 (AAV6) vector expressing recombinant fluorescent TMEM100 protein and injected it into the sciatic nerve (SN) of two pain models: CCI and TNI. PWMT and PWTL were significantly increased in the two groups, along with the expression of TMEM100 in the spinal cord and DRG. It also significantly inhibited the activation of microglia, astrocytes, and several inflammatory mediators (TNF- α, IL-1 β, and IL-6). In summary, the results of this study suggested that TMEM100 might be a promising molecular strategy for the treatment of NP, and its anti-inflammatory effects might play an important role in pain relief.

中文翻译：

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TMEM100 通过减少炎症因子的表达来调节神经性疼痛

对于周围神经损伤引起的慢性神经性疼痛（NP），目前尚无有效的治疗方法，这极大地影响了受影响者的生活质量。跨膜蛋白100（TMEM100）被认为是一种疼痛调节蛋白，在大鼠的背根神经节（DRG）中表达。然而，疼痛调节机制以及各种周围神经损伤后TMEM100的表达尚不清楚。在本研究中，我们构建了两种周围神经损伤的疼痛模型：胫神经损伤（TNI）和慢性压迫性损伤（CCI）。本研究发现，两种疼痛模型中大鼠的缩爪机械阈值（PWMT）和缩爪热潜伏期（PWTL）均显着降低，两组DRG中TMEM100的表达量也显着降低。此外，CCI组的下降比TNI组更明显。没有显着的统计学意义（）。我们构建了表达重组荧光 TMEM100 蛋白的腺相关病毒 6 (AAV6) 载体，并将其注射到两种疼痛模型：CCI 和 TNI 的坐骨神经 (SN) 中。两组的 PWMT 和 PWTL 以及脊髓和 DRG 中 TMEM100 的表达均显着增加。它还显着抑制小胶质细胞、星形胶质细胞和几种炎症介质（TNF- α、IL-1β和IL-6）的激活总之，这项研究的结果表明TMEM100可能是治疗NP的有前途的分子策略，其抗炎作用可能在缓解疼痛中发挥重要作用。