Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan.
Kaohsiung J Med Sci. 2013 Aug;29(8):405-11. doi: 10.1016/j.kjms.2012.12.001. Epub 2013 Feb 6.
To investigate whether 4-methylcatechol (4MC) could decrease the duration of the thermosensation disorder and promote the innervation of peptidergic intraepidermal nerve fibers (IENFs), we developed a resiniferatoxin (RTX)-induced neuropathic mouse model with thermal analgesia and skin denervation that was followed by daily 4MC treatment. On day 7 after RTX administration (RTXd7), the substance P (SP)(+) IENFs were completely depleted compared with the vehicle group (p < 0.0001), whereas the calcitonin gene-related peptide (CGRP)(+) IENFs were dramatically, but not completely, depleted (p < 0.0001). While SP(+) IENFs remained depleted (p = 0.0043), CGRP(+) IENFs were recovered by RTXd84 (p = 0.78). 4MC had no effect on the reinnervation of SP(+) IENFs, but markedly promoted the reinnervation of CGRP(+) IENFs on RTXd35 (p = 0.035). On RTXd56, CGRP(+) IENFs were comparable with the vehicle group (p = 0.39). In addition, 4MC normalized thermal analgesia on RTXd35 compared with RTX group (p = 0.007). In the current study, the significant promotion of reinnervation of CGRP(+) IENFs and thermal latencies on RTXd35 by 4MC indicated that CGRP(+) IENFs were responsible for the thermal transmission in chronic phase of RTX-induced neuropathy.
为了研究 4-甲基儿茶酚（4MC）是否可以缩短热感觉障碍的持续时间并促进肽能表皮内神经纤维（IENF）的神经支配，我们开发了一种树脂毒素（RTX）诱导的神经病理性小鼠模型，该模型具有热镇痛和皮肤去神经支配的特征，随后每天进行 4MC 治疗。在 RTX 给药后 7 天（RTXd7），与载体组相比，物质 P（SP）（+）IENF 完全耗尽（p <0.0001），而降钙素基因相关肽（CGRP）（+）IENF 则明显但不完全耗尽（p <0.0001）。虽然 SP（+）IENF 仍然耗尽（p = 0.0043），但 CGRP（+）IENF 在 RTXd84 时得到恢复（p = 0.78）。4MC 对 SP（+）IENF 的再支配没有影响，但在 RTXd35 时明显促进了 CGRP（+）IENF 的再支配（p = 0.035）。在 RTXd56 时，CGRP（+）IENF 与载体组相当（p = 0.39）。此外，与 RTX 组相比，4MC 在 RTXd35 时使热镇痛正常化（p = 0.007）。在本研究中，4MC 在 RTXd35 时对 CGRP（+）IENF 的再支配和热潜伏期的显著促进表明，CGRP（+）IENF 负责 RTX 诱导的神经病变慢性期的热传递。
