Department of Acupuncture, Moxibustion and Acupoint, College of Korean Medicine, Daegu Haany University, Daegu 42158, Korea.
Research Center for Herbal Convergence on Liver Disease, Daegu Haany University, Daegu 42158, Korea.
Int J Mol Sci. 2021 Mar 6;22(5):2672. doi: 10.3390/ijms22052672.
In the present study, we examined superoxide-mediated excitatory nociceptive transmission on at-level neuropathic pain following spinal thoracic 10 contusion injury (SCI) in male Sprague Dawley rats.
Mechanical sensitivity at body trunk, neuronal firing activity, and expression of superoxide marker/ionotropic glutamate receptors (iGluRs)/CamKII were measured in the T7/8 dorsal horn, respectively.
Topical treatment of superoxide donor t-BOOH (0.4 mg/kg) increased neuronal firing rates and pCamKII expression in the naïve group, whereas superoxide scavenger Tempol (1 mg/kg) and non-specific ROS scavenger PBN (3 mg/kg) decreased firing rates in the SCI group (* < 0.05). SCI showed increases of iGluRs-mediated neuronal firing rates and pCamKII expression (* < 0.05); however, t-BOOH treatment did not show significant changes in the naïve group. The mechanical sensitivity at the body trunk in the SCI group (6.2 ± 0.5) was attenuated by CamKII inhibitor KN-93 (50 μg, 3.9 ± 0.4) or Tempol (1 mg, 4 ± 0.4) treatment (* < 0.05). In addition, the level of superoxide marker Dhet showed significant increase in SCI rats compared to the sham group (11.7 ± 1.7 vs. 6.6 ± 1.5, * < 0.05).
Superoxide and the pCamKII pathway contribute to chronic at-level neuropathic pain without involvement of iGluRs following SCI.
在本研究中，我们研究了雄性 Sprague Dawley 大鼠胸 10 脊髓挫伤（SCI）后同节段神经病理性疼痛中的超氧化物介导的兴奋性伤害性传递。
分别测量躯体感觉、神经元放电活动和 T7/8 背角中超氧化物标志物/离子型谷氨酸受体（iGluRs）/CamKII 的表达。
局部给予超氧化物供体 t-BOOH（0.4 mg/kg）可增加正常组神经元的放电频率和 pCamKII 的表达，而超氧化物清除剂 Tempol（1 mg/kg）和非特异性 ROS 清除剂 PBN（3 mg/kg）可降低 SCI 组的放电频率（* < 0.05）。SCI 组 iGluRs 介导的神经元放电频率和 pCamKII 的表达增加（* < 0.05）；然而，t-BOOH 处理在正常组中没有显示出显著变化。SCI 组躯体感觉敏感性（6.2 ± 0.5）可被 CamKII 抑制剂 KN-93（50 μg，3.9 ± 0.4）或 Tempol（1 mg，4 ± 0.4）治疗所减弱（* < 0.05）。此外，与假手术组相比，SCI 大鼠中超氧化物标志物 Dhet 的水平显著升高（11.7 ± 1.7 对 6.6 ± 1.5，* < 0.05）。
超氧化物和 pCamKII 途径参与了 SCI 后慢性同节段神经病理性疼痛，而不涉及 iGluRs。
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