Cai Hui-Qian, Lin Xin-Ying, Chen Hai-Yan, Zhang Xi, Lin Yuan-Yuan, Pan Shan-Na, Qin Mei-Xiang, Su Sheng-Yong
Department of Rehabilitation, The First Affiliated Hospital, Guangxi University of Traditional Chinese Medicine, Nanning, Guangxi Province, China.
Department of First School of Clinical Medicine, Guangxi University of Traditional Chinese Medicine, Nanning, Guangxi Province, China.
Brain Behav. 2022 Apr;12(4):e2545. doi: 10.1002/brb3.2545. Epub 2022 Mar 22.
Direct moxibustion (DM) is reported to be useful for cervical spondylotic radiculopathy (CSR), but the analgesic mechanism remains unknown. Autophagy plays a protective role in neuronal apoptosis, Act A/Smads signaling pathway has been confirmed to be associated with the activation of autophagy. The study aimed to explore the effect of DM on autophagy in rats with CSR and the involvement of Act A/Smads signaling pathway.
Rats were randomly divided into Sham, CSR, CSR + DM, CSR + DM + 3-MA (PI3K inhibitor), and CSR + DM + SB (Act A inhibitor) group. Three days after establishment of CSR model with a fish line inserted under the axilla of the nerve roots, DM at Dazhui (GV14) was performed six times once for seven consecutive days. Western blot and immunofluorescence staining were used to observe the expression of the neuronal autophagy molecule LC3II/I, Atg7, and Act A/Smads signaling molecule Act A, p-Smad2, and p-Smad3. Bcl-2/Bax mRNA expression was measured by real time PCR.
DM improved the pain threshold and motor function of CSR rats and promoted the expression of Act A, p-Smad2, p-Smad3, LC3II/I, and Atg7 in the entrapped-nerve root spinal dorsal horn. DM reduced the expression of Bax mRNA and decreased the number of apoptotic neurons. 3-MA and Act A inhibitor SB suppressed the expression of above-mentioned proteins and reduced the protective effect of DM on apoptotic neurons.
DM exerts analgesic effects by regulating the autophagy to reduce cell apoptosis and repair nerve injury, and this feature may be related to the Act A/Smads signaling pathway.
据报道，直接灸对神经根型颈椎病（CSR）有效，但镇痛机制尚不清楚。自噬在神经元凋亡中起保护作用，已证实激活素A/ Smads信号通路与自噬的激活有关。本研究旨在探讨直接灸对CSR大鼠自噬的影响以及激活素A/ Smads信号通路的参与情况。
将大鼠随机分为假手术组、CSR组、CSR + 直接灸组、CSR + 直接灸 + 3-MA（PI3K抑制剂）组和CSR + 直接灸 + SB（激活素A抑制剂）组。在神经根腋窝下插入鱼线建立CSR模型三天后，于大椎穴（GV14）进行直接灸，连续七天，每天一次，共六次。采用蛋白质免疫印迹法和免疫荧光染色法观察神经元自噬分子LC3II/I、Atg7以及激活素A/ Smads信号分子激活素A、p-Smad2和p-Smad3的表达。通过实时PCR检测Bcl-2/Bax mRNA表达。
直接灸提高了CSR大鼠的痛阈和运动功能，促进了卡压神经根脊髓背角中激活素A、p-Smad2、p-Smad3、LC3II/I和Atg7的表达。直接灸降低了Bax mRNA的表达，减少了凋亡神经元的数量。3-MA和激活素A抑制剂SB抑制了上述蛋白的表达，降低了直接灸对凋亡神经元的保护作用。
直接灸通过调节自噬以减少细胞凋亡和修复神经损伤发挥镇痛作用，这一作用可能与激活素A/ Smads信号通路有关。
