小鼠术后慢性疼痛期间TRPV1与PI3K/AKT/mTOR通路的脊髓受累情况
Spinal Involvement of TRPV1 and PI3K/AKT/mTOR Pathway During Chronic Postoperative Pain in Mice.
作者信息
Santos Gabriela Xavier, Dos Anjos-Garcia Tayllon, Vieira Ana Carolina de Jesus, Galdino Giovane
机构信息
Center for Experimental Biology, Laboratory of Neuroimmunobiology of Pain, Federal University of Alfenas, Alfenas 37133-840, MG, Brazil.
Inapós College, Padre Gervásio National Institute of Higher Education and Postgraduate Studies, Pouso Alegre 37550-121, MG, Brazil.
出版信息
Brain Sci. 2025 Jan 8;15(1):53. doi: 10.3390/brainsci15010053.
BACKGROUND
Chronic postoperative pain (CPOP) is among the main consequences of surgical procedures, directly affecting the quality of life. Although many strategies have been used to treat this symptom, they are often ineffective. Thus, studies investigating CPOP-associated mechanisms may help to develop more effective treatment strategies. Therefore, the present study investigated the spinal participation of the transient potential receptor vanilloid type 1 (TRPV1) and PI3K/AKT/mTOR pathway activation during CPOP.
METHODS
In this study C57BL/6 male mice were used, and CPOP was induced by muscle retraction and incision. The nociceptive threshold was measured by the von Frey filament test. For pharmacological evaluation, TRPV1 and PI3K/AKT/mTOR inhibitors were administered intrathecally. TRPV1 and PI3K/AKT/mTOR protein levels were evaluated by Western blotting.
RESULTS
The results showed that CPOP increased TRPV1 and mTOR protein levels, and pretreatment with the specific inhibitors alleviated CPOP. In addition, pretreatment with the TRPV1 antagonist SB-366791 attenuated mTOR protein levels.
CONCLUSIONS
The results suggest that TRPV1 and the PI3K/AKT/mTOR pathway are involved in CPOP at the spinal level, and TRPV1 may activate mTOR during this process.
背景
慢性术后疼痛（CPOP）是外科手术的主要后果之一，直接影响生活质量。尽管已采用多种策略来治疗这种症状，但往往效果不佳。因此，研究CPOP相关机制可能有助于制定更有效的治疗策略。因此，本研究调查了CPOP期间瞬时受体电位香草酸亚型1（TRPV1）和PI3K/AKT/mTOR通路激活在脊髓中的作用。
方法
本研究使用C57BL/6雄性小鼠，通过肌肉牵拉和切开诱导CPOP。用von Frey细丝试验测量痛觉阈值。为进行药理学评估，鞘内注射TRPV1和PI3K/AKT/mTOR抑制剂。通过蛋白质印迹法评估TRPV1和PI3K/AKT/mTOR蛋白水平。
结果
结果表明，CPOP增加了TRPV1和mTOR蛋白水平，用特异性抑制剂预处理可减轻CPOP。此外，用TRPV1拮抗剂SB-366791预处理可降低mTOR蛋白水平。
结论
结果表明，TRPV1和PI3K/AKT/mTOR通路在脊髓水平参与CPOP，并且在此过程中TRPV1可能激活mTOR。
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