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[1]鄭軍凡,林愛金,桂鋒,等.過表達(dá)Pdk4對脊神經(jīng)結(jié)扎小鼠線粒體及神經(jīng)元電生理活性的影響[J].福建醫(yī)藥雜志,2025,47(01):73-77.[doi:10.20148/j.fmj.2025.01.023]
　ZHENG Junfan,LIN Aijin,GUI Feng,et al.Effects of Pdk4 overexpression on mitochondrial and neuronal electrophy-siological activities in spinal nerve ligation mice[J].FUJIAN MEDICAL JOURNAL,2025,47(01):73-77.[doi:10.20148/j.fmj.2025.01.023]
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過表達(dá)Pdk4對脊神經(jīng)結(jié)扎小鼠線粒體及神經(jīng)元電生理活性的影響()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
47
期數(shù):
2025年01期
頁碼:
73-77
欄目:
基礎(chǔ)研究
出版日期:
2025-01-20

文章信息/Info

Title:
Effects of Pdk4 overexpression on mitochondrial and neuronal electrophy-siological activities in spinal nerve ligation mice
文章編號:
1002-2600(2025)01-0073-05
作者:
鄭軍凡; 林愛金; 桂鋒; 陳述榮; 陳昕
福建省福州市第二總醫(yī)院康復(fù)一科,福州 350007
Author(s):
ZHENG Junfan;  LIN Aijin;  GUI Feng;  CHEN Shurong;  CHEN Xin
The First Department of Rehabilitation, Fuzhou Second General Hospital, Fuzhou, Fujian 350007, China
關(guān)鍵詞:
脊神經(jīng);  線粒體;  神經(jīng)元;  電生理
Keywords:
spinal nerve;  mitochondria;  neuron;  electrophysiology
分類號:
R329.2
DOI:
10.20148/j.fmj.2025.01.023
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 考察過表達(dá)丙酮酸脫氫酶激酶 4(Pdk4)對脊神經(jīng)結(jié)扎小鼠線粒體及神經(jīng)元電生理活性的影響,進(jìn)一步揭示神經(jīng)病理性疼痛的發(fā)病機(jī)制。方法 選用雄性C57BL/6小鼠構(gòu)建脊神經(jīng)結(jié)扎(SNL)模型并分為假手術(shù)組、SNL模型組及SNL模型+Pdk4過表達(dá)組。SNL模型+Pdk4過表達(dá)組采用脊髓背角內(nèi)病毒注射法注射Pdk4過表達(dá)病毒。采用不同規(guī)格細(xì)絲檢測足底機(jī)械性疼痛閾值; 采用Western blot測定小鼠脊髓背角Pdk4、LC3-Ⅱ、LC3-Ⅰ蛋白表達(dá); 采用電子顯微鏡觀察線粒體形態(tài); 采用膜片鉗技術(shù)測定神經(jīng)元電生理指標(biāo)。結(jié)果 過表達(dá)Pdk4后,小鼠機(jī)械性疼痛閾值降低(P<0.05); 透射電鏡觀察顯示線粒體腫脹更明顯,嵴結(jié)構(gòu)進(jìn)一步紊亂且部分出現(xiàn)空泡化; Pdk4蛋白表達(dá)量升高(P<0.05),LC3-Ⅱ/LC3-I比值升高(P<0.05); 小鼠脊髓背角內(nèi)神經(jīng)元自發(fā)性興奮性突觸后電流增大,動(dòng)作電位釋放個(gè)數(shù)增多,基強(qiáng)度降低,輸入阻抗降低(P<0.05)。結(jié)論 Pdk4表達(dá)上調(diào)使小鼠疼痛閾值降低,增加疼痛敏感性,可能與脊髓背角線粒體形態(tài)變化、自噬相關(guān)信號通路激活及神經(jīng)元興奮性增強(qiáng)有關(guān)。
Abstract:
Objective To investigate the effects of Pdk4 overexpression on mitochondrial and neuronal electrophysiologi-cal activities in spinal nerve ligation mice, and to further reveal the pathogenesis of neuropathic pain. Methods Male C57BL/6 mice were selected to establish the spinal nerve ligation model, and they were divided into the sham-operation group, the SNL model group, and the SNL model+Pdk4 overexpression group. The SNL model+Pdk4 overexpression group was injected with Pdk4-overexpressing virus by intraspinal dorsal horn viral injection. Filaments of different specifications were used to detect the plantar mechanical pain threshold. Western blot was used to determine the protein expressions of Pdk4, LC3-Ⅱ, and LC3-I in the spinal dorsal horn of mice. Electron microscope was used to observe the mitochondrial morphology. The patch-clamp technique was used to measure the neuronal electrophysiological indexes. Results After Pdk4 overexpression, the mechanical pain threshold of mice decreased(P<0.05). Transmission electron microscopy showed more obvious mitochondrial swelling, further disorder of the cristae structure, and partial vacuolization. The expression level of Pdk4 protein increased(P<0.05), and the ratio of LC3-Ⅱ/LC3-I increased(P<0.05). In the spinal dorsal horn of mice, the spontaneous excitatory postsynaptic current of neurons increased, the number of action potential releases increased, the rheobase decreased, and the input impedance decreased(P<0.05).Conclusion The up-regulation of Pdk4 expression reduces the pain threshold of mice and increases pain sensitivity, which may be related to the morphological changes of mitochondria in the spinal dorsal horn, the activation of autophagy-related signaling pathways, and the enhancement of neuronal excitability.

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備注/Memo

備注/Memo:
基金項(xiàng)目:2023年福州市衛(wèi)健系統(tǒng)科技計(jì)劃中青年科研項(xiàng)目(2023-S-wq10); 福建省創(chuàng)傷骨科急救與康復(fù)臨床醫(yī)學(xué)研究中心項(xiàng)目(2020Y2014)
更新日期/Last Update: 2025-01-20