| 李芝,葛玲玲,刘佩萱,等.浓缩生长因子对大鼠正畸牙齿运动引起的口面疼痛作用及对降钙素基因相关肽表达的影响[J].安徽医药,2026,30(7):1339-1344. |
| 浓缩生长因子对大鼠正畸牙齿运动引起的口面疼痛作用及对降钙素基因相关肽表达的影响 |
| Effects of CGF on orofacial pain induced by orthodontic tooth movement and on CGRP expression in rats |
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| DOI：10.3969/j.issn.1009-6469.2026.07.013 |
| 中文关键词: 面部疼痛 浓缩生长因子( CGF) 降钙素基因相关肽( CGRP) 正畸牙齿运动 三叉神经节 大鼠， Sprague-Dawley |
| 英文关键词: Facial pain Concentrated growth factors (CGF) Calcitonin gene-related peptide (CGRP) Orthodontic tooth move-ment Trigeminal ganglion Rats,Sprague-Dawley |
| 基金项目:河北省医学科学研究课题计划项目( 20231102) |
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| 中文摘要: |
| 目的探讨浓缩生长因子(CGF)是否通过调控降钙素基因相关肽(CGRP)的表达对实验性大鼠正畸牙齿运动引起的口面疼痛的影响。方法研究时间为 2023年 6月至 2024年 6月。在 Sprague-Dawley大鼠的切牙和磨牙之间结扎闭合式螺旋弹簧引起口面部疼痛；通过实时聚合酶链反应、免疫荧光染色和荧光原位杂交测定基因和蛋白表达水平；利用携带 Atp6v0a1 shRNA的慢病毒载体敲低 TG和人神经母细胞瘤细胞(SH-SY5Y)神经元中 Atp6v0a1的表达；用荧光染料 FM1-43观察 SH-SY5Y神经元内囊泡的释放，用酶联免疫吸附分析检测 CGRP的释放；口面部疼痛通过大鼠颌面部疼痛量表进行评估。结果神经节内给予 CGF可上调三叉神经节(TG)和三叉神经脊束核尾侧亚核(VC)中的 CGRP的表达，而给予 Atp6v0a1 shRNA则可下调其表达。口面部疼痛评分(RGS)结果显示，对照组、 CGF组及 anti-CGF组分别为(2.98±0.36)分、(3.78±0.42)分和(2.41±0.29)分，差异有统计学意义(P<0.05)。VC中 CGRP表达水平(术后 3d)在三组间差异有统计学意义(P<0.05)。体外实验中， CGF组的细胞上清液 CGRP浓度显著高于其他两组(P<0.001)。CGF组 FM1-43荧光强度(反映囊泡释放)显著高于其他两组(P<0.001)。此外， CGF+Atp6v0a1 shRNA组较 CGF+NC组显著降低 CGRP释放和囊泡释放(P<0.001)。结论在实验性牙移动引起的口面疼痛中， CGF诱导了 TG和 VC中 CGRP的上调，且这一过程依赖于 Atp6v0a1和囊泡的释放，提示它们参与了口面部疼痛中伤害性信息的传递。 |
| 英文摘要: |
| Objective To investigate whether concentrated growth factors (CGF) influence orofacial pain induced by orthodontic toothmovement in experimental rats by regulating the expression of calcitonin gene-related peptide (CGRP).Methods The research period was from June 2023 to June 2024. Ligation of a closed coil spring between the incisors and molars of Sprague-Dawley rats caused orofa-cial pain. Gene and protein expression levels were determined by real-time polymerase chain reaction, immunofluorescence stainingand fluorescence in situ hybridization. The expression of Atp6v0a1 in TG and SH-SY5Y neurons was knocked down by lentiviral vector carrying Atp6v0a1 shRNA. The release of vesicles in SH-SY5Y neurons was observed by fluorescent dye FM1-43, and the release of CGRP was detected by enzyme-linked immunosorbent assay. Oral and facial pain was assessed by the rat maxillofacial pain scale.Re. sults The study showed that intraganglionic administration of CGF upregulated, whereas Atp6v0a1 shRNA downregulated, the expres-sion of CGRP in the trigeminal ganglion (TG) and the spinal trigeminal nucleus caudalis (VC). The RGS scores for facial pain were(2.98±0.36), (3.78±0.42), and (2.41±0.29) points in the control, CGF, and anti-CGF groups, respectively, with statistically significant differences among groups (P<0.05). The expression levels of CGRP in the VC on day 3 in the control, CGF, and anti-CGF groups, re-spectively (P<0.05 for comparisons). In vitro, the concentrations of CGRP in the cell supernatant of SH-SY5Y neurons in the control, CGF, and anti-CGF groups, respectively; the CGF group was significantly higher than the other two groups (P<0.001). The FM1-43 fluo-rescence intensity (reflecting vesicle release) in the control, CGF, and anti-CGF groups, respectively; the CGF group was significantly higher than the other two groups (P<0.001). Furthermore, the CGF+Atp6v0a1 shRNA group showed significantly lower CGRP release and vesicle release (P<0.001) compared with the CGF+NC group.Conclusion In the oral and facial pain induced by experimental tooth movement, CGF induced the up-regulation of CGRP in TG and VC, and this process depended on the release of Atp6v0a1 andvesicles, suggesting that they were involved in the transmission of nociceptive information in oral and facial pain. |
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