高频及低频重复经颅磁刺激对急性一氧化碳中毒迟发性脑病的疗效

doi:10.3877/cma.j.issn.2095-123X.2025.04.002

目的

观察高频及低频重复经颅磁刺激（rTMS）治疗对急性一氧化碳（CO）中毒迟发性脑病（DEACMP）实验鼠的脑源性神经营养因子(BDNF)/酪氨酸激酶受体B（TrkB）信号通路的表达及MBP含量的影响并探讨疗效。

方法

采用Morris水迷宫筛选出24只认知合格的SD大鼠，采用随机数字表法选取6只为空白组（NC组），余18只建立DEACMP模型后随机分为假刺激组（Sham组）、高频治疗组（5 Hz组）及低频治疗组（1 Hz组），每组6只。高频、低频治疗组分别给予5、1 Hz rTMS治疗，Sham组给予假刺激。治疗后通过Morris水迷宫评估实验鼠的认知功能。采用苏木素-伊红（HE）染色法观察实验鼠海马区的损伤情况，酶联免疫吸附法（ELISA）分析BDNF、TrkB、髓鞘碱性蛋白质（MBP）血清浓度，免疫组织化学（IHC）染色法检测BDNF、TrkB、MBP阳性表达。

结果

（1）Morris水迷宫结果：CO中毒21 d，平均逃避潜伏期比较，NC组<5 Hz组<1 Hz组<Sham组，差异均有统计学意义（P<0.05）。（2）HE染色结果：NC组海马区细胞排列齐整、界清且胞数正常，Sham组海马区细胞排列紊乱、胞数减少且部分出现核固缩坏死，1 Hz组、5 Hz组海马区细胞排列较为齐整，偶有细胞坏死。（3）ELISA分析结果：与NC组相比，Sham组的BDNF和TrkB表达含量降低，MBP表达含量上升，差异均有统计学意义（P<0.05）；1 Hz组和5 Hz组的BDNF、TrkB表达含量较Sham组明显上升，MBP表达含量较Sham组明显降低，差异均有统计学意义（P<0.05）。（4）IHC染色结果：与NC组相比，Sham组中BDNF和TrkB的平均光密度值降低，差异均有统计学意义（P<0.05）；1 Hz组和5 Hz组BDNF、TrkB的平均光密度值均高于Sham组，差异均有统计学意义（P<0.05）；Sham组的MBP平均光密度值明显高于NC组，1 Hz组和5 Hz组的MBP平均光密度值均低于Sham组，差异均有统计学意义（P<0.05）。

结论

高频（5 Hz）和低频（1 Hz）的rTMS均可改善DEACMP实验鼠的认知功能，可能作用机制是通过上调BDNF/TrkB通路表达改善脱髓鞘病变，使MBP的表达含量降低，从而提升认知能力。

关键词: 重复经颅磁刺激, 急性一氧化碳中毒迟发性脑病, 脑源性神经营养因子, 酪氨酸激酶受体B, 髓鞘碱性蛋白

Objective

To observe the effects of high-frequency and low-frequency repetitive transcranial magnetic stimulation (rTMS) treatment on the expression of brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signalling pathway and MBP content in rats with delayed encephalopathy in acute carbon monoxide poisoning (DEACMP) and to explore the therapeutic effects.

Methods

Cognitively qualified male 24 SD rats were screened by Morris water maze, 6 were randomly selected as the blank group (NC group), and 18 were randomly divided into the sham stimulation group (Sham group), the high frequency 5 Hz group (5 Hz group), and the low frequency 1 Hz group (1 Hz group), each with 6 rats in each group, after the establishment of the DEACMP model. The treatment group was given 5 Hz and 1 Hz rTMS treatment respectively, and the Sham group was given sham stimulation. Cognitive function was assessed by Morris water maze after treatment. Hematoxylin-eosin (HE) staining was used to observe the changes in the hippocampal region of rats; enzyme-linked immunosorbent assay (ELISA) was used to analyse the serum concentration of BDNF, TrkB and myelin basic protein (MBP); immunohistochemical staining (IHC) was used to detect the positive expression of BDNF, TrkB and MBP in each group.

Results

(1) The results of Morris water maze showed that 21 d after CO poisoning, the mean avoidance latency was significantly longer in the Sham group, 1 Hz group and 5 Hz group compared with the NC group (P<0.05); the mean avoidance latency was significantly shorter in the 1 Hz and 5 Hz groups compared with that in the Sham group (P<0.05); and the mean avoidance latency was even shorter in the 5 Hz group compared with that in the 1 Hz group (P<0.05). (2) The results of HE staining showed that the cells in the hippocampus of the NC group were neatly arranged, with clear boundaries and normal cell number, while the cells in the hippocampus of the Sham group were disorganised, with a reduced cell number and some of them showed nuclear necrosis. The hippocampal area of the 1 Hz and 5 Hz groups was more neatly arranged, with occasional cell necrosis. (3) The ELISA results indicated that compared with the NC group, the expression content of BDNF and TrkB in the Sham group decreased, and the expression content of MBP increased (P<0.05); in the 1 Hz and 5 Hz groups, the expression content of BDNF and TrkB increased significantly compared with that of the Sham group, and the expression content of MBP increased significantly compared with that of the Sham group. MBP expression content was significantly lower than that in the Sham group (P<0.05). (4) IHC staining indicated that the mean optical density values of BDNF and TrkB in the Sham group were decreased compared with that in the NC group (P<0.05); the mean optical density values of BDNF and TrkB in both the 1 Hz group and the 5 Hz group were higher than that in the Sham group (P<0.05); the MBP mean optical density values of BDNF and TrkB in the Sham group and the 5 Hz group were higher than those in the Sham group (P<0.05); the mean optical density values of MBP in the Sham group were significantly higher than those in the NC group, and the mean optical density values of MBP in the 1 Hz and 5 Hz groups were lower than those in the Sham group (P<0.05).

Conclusions

Both high-frequency (5 Hz) and low-frequency (1 Hz) rTMS can improve the cognitive function of DEACMP mice, and the possible mechanism is to improve demyelinating lesions by up-regulating the expression of BDNF/TrkB pathway, so as to reduce the expression content of MBP, thus improving cognitive ability.

Key words: Repetitive transcranial magnetic stimulation, Acute carbon monoxide poisoning delayed encephalopathy, Brain-derived neurotrophic factor, Tyrosine kinase receptor B, Myelin basic protein

表1 4组实验鼠Morris水迷宫平均逃避潜伏期比较（s，mean±SD）

Tab.1 Comparison of average escape latency in Morris water maze among 4 groups (s, mean±SD)

组别	只数	中毒21 d	治疗14 d	t值	P值
NC组	6	11.62±0.98	12.52±0.72	1.623	0.166
Sham组	6	33.96±3.14^a	33.23±3.95^a	0.614	0.566
1 Hz组	6	34.03±2.28^a	29.99±1.84^ab	4.074	0.010
5 Hz组	6	34.02±3.06^a	25.52±1.19^abc	10.026	<0.001
F值		118.291	94.989
P值		<0.001	<0.001

表1 4组实验鼠Morris水迷宫平均逃避潜伏期比较（s，mean±SD）

Tab.1 Comparison of average escape latency in Morris water maze among 4 groups (s, mean±SD)

组别	只数	中毒21 d	治疗14 d	t值	P值
NC组	6	11.62±0.98	12.52±0.72	1.623	0.166
Sham组	6	33.96±3.14^a	33.23±3.95^a	0.614	0.566
1 Hz组	6	34.03±2.28^a	29.99±1.84^ab	4.074	0.010
5 Hz组	6	34.02±3.06^a	25.52±1.19^abc	10.026	<0.001
F值		118.291	94.989
P值		<0.001	<0.001

图1 4组实验鼠脑海马组织HE染色结果（×200）A：NC组；B：Sham组，大部分核出现固缩坏死（箭头所示)；C~D：1 Hz组（C）和5 Hz组（D）偶见细胞坏死（箭头所示)

Fig.1 HE staining results of hippocampal tissue in 4 groups (×200)

表2 4组实验鼠血清中BDNF、TrkB、MBP表达水平比较（ng/mL，mean±SD）

Tab.2 Expression levels of BDNF, TrkB and MBP in serum of experimental rats (ng/mL, mean±SD)

组别	只数	BDNF	TrkB	MBP
NC组	6	18.28±0.66	408.05±23.35	217.20±55.20
Sham组	6	16.84±1.12^a	380.64±16.81^a	337.77±55.52^a
1 Hz组	6	19.32±1.49^b	424.26±20.37^b	243.23±42.18^b
5 Hz组	6	19.20±1.33^b	422.81±24.99^b	253.86±43.81^b
F值		5.539	5.266	6.645
P值		0.006	0.008	0.003

表2 4组实验鼠血清中BDNF、TrkB、MBP表达水平比较（ng/mL，mean±SD）

Tab.2 Expression levels of BDNF, TrkB and MBP in serum of experimental rats (ng/mL, mean±SD)

组别	只数	BDNF	TrkB	MBP
NC组	6	18.28±0.66	408.05±23.35	217.20±55.20
Sham组	6	16.84±1.12^a	380.64±16.81^a	337.77±55.52^a
1 Hz组	6	19.32±1.49^b	424.26±20.37^b	243.23±42.18^b
5 Hz组	6	19.20±1.33^b	422.81±24.99^b	253.86±43.81^b
F值		5.539	5.266	6.645
P值		0.006	0.008	0.003

表3 4组实验鼠rTMS治疗14 d后海马组织BDNF、TrkB、MBP的平均光密度值比较（mean±SD）

Tab.3 Comparison of the average optical density of BDNF, TrkB and MBP in hippocampus of four groups of experimental rats after rTMS treatment for 14 d (mean±SD)

组别	只数	BDNF	TrkB	MBP
NC组	6	31.46±0.45	32.19±1.67	23.75±0.97
Sham组	6	28.21±1.18^a	29.00±1.03^a	26.20±0.99^a
1 Hz组	6	30.42±1.86^b	30.50±1.05^ab	24.91±0.67^ab
5 Hz组	6	30.08±0.74^b	31.44±0.58^b	24.05±0.84^b
F值		7.872	8.592	9.424
P值		0.001	0.001	<0.001

表3 4组实验鼠rTMS治疗14 d后海马组织BDNF、TrkB、MBP的平均光密度值比较（mean±SD）

Tab.3 Comparison of the average optical density of BDNF, TrkB and MBP in hippocampus of four groups of experimental rats after rTMS treatment for 14 d (mean±SD)

组别	只数	BDNF	TrkB	MBP
NC组	6	31.46±0.45	32.19±1.67	23.75±0.97
Sham组	6	28.21±1.18^a	29.00±1.03^a	26.20±0.99^a
1 Hz组	6	30.42±1.86^b	30.50±1.05^ab	24.91±0.67^ab
5 Hz组	6	30.08±0.74^b	31.44±0.58^b	24.05±0.84^b
F值		7.872	8.592	9.424
P值		0.001	0.001	<0.001

图2 IHC检测4组实验鼠rTMS治疗14 d后海马组织BDNF表达水平（×200）A：NC组；B：Sham组；C：1 Hz组；D：5 Hz组；HE染色中胞核为蓝色，DAB染色中阳性表达呈现棕黄色；箭头所示为BDNF的阳性表达；BDNF：脑源性神经营养因子；rTMS：重复经颅磁刺激；IHC：免疫组织化学

Fig.2 IHC was used to detect BDNF expression in hippocampus of four groups of experimental rats after rTMS treatment for 14 d (×200)

图3 IHC检测4组实验鼠rTMS治疗14 d后海马组织TrkB表达水平（×200）A：NC组；B：Sham组；C：1 Hz组；D：5 Hz组；HE染色中胞核为蓝色，DAB染色中阳性表达呈现棕黄色；箭头所示为TrkB的阳性表达；TrkB：酪氨酸激酶受体B；rTMS：重复经颅磁刺激；IHC：免疫组织化学

Fig.3 IHC was used to detect TrkB expression in hippocampus of four groups of experimental rats after rTMS treatment for 14 d (×200)

图4 IHC检测4组实验鼠rTMS治疗14 d后海马组织MBP表达水平（×200）A：NC组；B：Sham组；C：1 Hz组；D：5 Hz组；HE染色中胞核为蓝色，DAB染色中阳性表达呈现棕黄色；箭头所示为MBP的阳性表达；MBP：髓鞘碱性蛋白质；rTMS：重复经颅磁刺激；IHC：免疫组织化学

Fig.4 IHC was used to detect MBP expression in hippocampus of four groups of experimental rats after rTMS treatment for 14 d (×200)

[1]	Lu B, Nagappan G, Lu Y. BDNF and synaptic plasticity, cognitive function, and dysfunction[J]. Handb Exp Pharmacol, 2014, 220: 223-250. DOI: 10.1007/978-3-642-45106-5_9.
[2]	张勇，周丽，何斌. BDNF Val66Met基因多态性对急性一氧化碳中毒迟发性脑病患者疗效的影响[J]. 中华脑科疾病与康复杂志(电子版), 2022, 12(6): 355-359. DOI: 10.3877/cma.j.issn.2095-123X.2022.06.007.
[3]	Shang Y, Wang X, Shang X, et al. Repetitive transcranial magnetic stimulation effectively facilitates spatial cognition and synaptic plasticity associated with increasing the levels of BDNF and synaptic proteins in Wistar rats[J]. Neurobiol Learn Mem, 2016, 134 Pt B: 369-378. DOI: 10.1016/j.nlm.2016.08.016.
[4]	马良飞，尹翎，方婷, 等. 重复经颅磁刺激联合虚拟现实技术对脑卒中后认知障碍的影响[J]. 中华脑科疾病与康复杂志(电子版), 2023, 13(6): 346-351. DOI: 10.3877/cma.j.issn.2095-123X.2023.06.005.
[5]	宋冰，辜吉秀，汪永锋, 等. 实验动物替代技术研究[J]. 中国实验动物学报, 2020, 28(5): 680-687. DOI: 10.3969/j.issn.1005-4847.2020.05.014.
[6]	陈超，王宝军，项文平, 等. 吸入法建立急性一氧化碳中毒迟发型脑病大鼠模型[J]. 中国医药导报, 2019, 16(15): 4-7.
[7]	Chernov AV, Hullugundi SK, Eddinger KA, et al. A myelin basic protein fragment induces sexually dimorphic transcriptome signatures of neuropathic pain in mice[J]. J Biol Chem, 2020, 295(31): 10807-10821. DOI: 10.1074/jbc.RA120.013696.
[8]	Ochi S, Abe M, Li C, et al. The nicotinic cholinergic system is affected in rats with delayed carbon monoxide encephalopathy[J]. Neurosci Lett, 2014, 569: 33-37. DOI: 10.1016/j.neulet.2014.03.054.
[9]	Zhang C, Lu R, Wang L, et al. Restraint devices for repetitive transcranial magnetic stimulation in mice and rats[J]. Brain Behav, 2019, 9(6): e01305. DOI: 10.1002/brb3.1305.
[10]	Luo J, Zheng H, Zhang L, et al. High-frequency repetitive transcranial magnetic stimulation (rTMS) improves functional recovery by enhancing neurogenesis and activating BDNF/TrkB signaling in ischemic rats[J]. Int J Mol Sci, 2017, 18(2): 455. DOI: 10.3390/ijms18020455.
[11]	Han S, Nah S, Choi S, et al. Optimal sessions of hyperbaric oxygen therapy in patients with carbon monoxide poisoning: a prospective observational study[J]. Am J Emerg Med, 2021, 44: 132-136. DOI: 10.1016/j.ajem.2020.10.062.
[12]	Chen SY, Lin CC, Lin YT, et al. Reversible changes of brain perfusion SPECT for carbon monoxide poisoning-induced severe akinetic mutism[J]. Clin Nucl Med, 2016, 41(5): e221-e227. DOI: 10.1097/rlu.0000000000001121.
[13]	Hara S, Mizukami H, Kurosaki K, et al. Existence of a threshold for hydroxyl radical generation independent of hypoxia in rat striatum during carbon monoxide poisoning[J]. Arch Toxicol, 2011, 85(9): 1091-1099. DOI: 10.1007/s00204-010-0637-2.
[14]	Chen J, Fan Y, Wei W, et al. Repetitive transcranial magnetic stimulation modulates cortical-subcortical connectivity in sensorimotor network[J]. Eur J Neurosci, 2022, 55(1): 227-243. DOI: 10.1111/ejn.15571.
[15]	Beynel L, Powers JP, Appelbaum LG. Effects of repetitive transcranial magnetic stimulation on resting-state connectivity: a systematic review[J]. Neuroimage, 2020, 211: 116596. DOI: 10.1016/j.neuroimage.2020.116596.
[16]	Chen X, Chen A, Wei J, et al. Dexmedetomidine alleviates cognitive impairment by promoting hippocampal neurogenesis via BDNF/TrkB/CREB signaling pathway in hypoxic-ischemic neonatal rats[J]. CNS Neurosci Ther, 2024, 30(1): e14486. DOI: 10.1111/cns.14486.
[17]	Jurič DM, Šuput D, Brvar M. Hyperbaric oxygen preserves neurotrophic activity of carbon monoxide-exposed astrocytes[J]. Toxicol Lett, 2016, 253: 1-6. DOI: 10.1016/j.toxlet.2016.04.019.
[18]	Li Q, Song JJ, Zhang HY, et al. Dexamethasone therapy for preventing delayed encephalopathy after carbon monoxide poisoning [J]. Biotech Histochem, 2015, 90(8): 561-567. DOI: 10.3109/10520295.2015.1019565.
[19]	Fletcher JL, Murray SS, Xiao J. Brain-derived neurotrophic factor in central nervous system myelination: a new mechanism to promote myelin plasticity and repair[J]. Int J Mol Sci, 2018, 19(12): 4131. DOI: 10.3390/ijms19124131.
[20]	Rubin L, Stabler CT, Schumacher-Klinger A, et al. Neurotrophic factors and their receptors in lung development and implications in lung diseases[J]. Cytokine Growth Factor Rev, 2021, 59: 84-94. DOI: 10.1016/j.cytogfr.2021.01.008.
[21]	Zhang F, Zeng J, Zhang X, et al. Investigation of the relationship between MBP gene polymorphisms and delayed encephalopathy after acute carbon monoxide poisoning[J]. Neurotoxicology, 2023, 94: 217-222. DOI: 10.1016/j.neuro.2022.12.002.
[22]	Xu L, Liu X, Guo C, et al. Inhibition of ROCK2 kinase activity improved behavioral deficits and reduced neuron damage in a DEACMP rat model[J]. Brain Res Bull, 2022, 180: 24-30. DOI: 10.1016/j.brainresbull.2021.12.018.
[23]	Fulmer CG, VonDran MW, Stillman AA, et al. Astrocyte-derived BDNF supports myelin protein synthesis after cuprizone-induced demyelination[J]. J Neurosci, 2014, 34(24): 8186-8196. DOI: 10.1523/jneurosci.4267-13.2014.
[24]	Huang Y, Song YJ, Isaac M, et al. Tropomyosin receptor kinase B expressed in oligodendrocyte lineage cells functions to promote myelin following a demyelinating lesion[J]. ASN Neuro, 2020, 12: 1759091420957464. DOI: 10.1177/1759091420957464.
[25]	El Khoury D. Study of myelin gene expression in the central nervous system using real-time PCR[J]. Methods Mol Biol, 2019, 2011: 659-670. DOI: 10.1007/978-1-4939-9554-7_38.
[26]	Antonijevic M, Dallemagne P, Rochais C. Inducing neuronal regeneration and differentiation via the BDNF/TrkB signaling pathway: a key target against neurodegenerative diseases?[J]. Neural Regen Res, 2024, 19(3): 495-496. DOI: 10.4103/1673-5374.380896.
[27]	Yang L, Su Y, Guo F, et al. Deep rTMS mitigates behavioral and neuropathologic anomalies in cuprizone-exposed mice through reducing microglial proinflammatory cytokines[J]. Front Integr Neurosci, 2020, 14: 556839. DOI: 10.3389/fnint.2020.556839.
[28]	Hou G, Gao M, Zheng Y, et al. Nomogram for stratifying patients with lifelong premature ejaculation before using the PHQ-9: an observational study[J]. Eur J Clin Invest, 2022, 52(9): e13809. DOI: 10.1111/eci.13809.
[29]	Wang F, Chang GM, Yu Q, et al. The neuroprotection of repetitive transcranial magnetic stimulation pre-treatment in vascular dementia rats[J]. J Mol Neurosci, 2015, 56(1): 198-204. DOI: 10.1007/s12031-014-0480-7.
[30]	Ma J, Zhang Z, Su Y, et al. Magnetic stimulation modulates structural synaptic plasticity and regulates BDNF-TrkB signal pathway in cultured hippocampal neurons[J]. Neurochem Int, 2013, 62(1): 84-91. DOI: 10.1016/j.neuint.2012.11.010.
[31]	Delarue Q, Robac A, Massardier R, et al. Comparison of the effects of two therapeutic strategies based on olfactory ensheathing cell transplantation and repetitive magnetic stimulation after spinal cord injury in female mice[J]. J Neurosci Res, 2021, 99(7): 1835-1849. DOI: 10.1002/jnr.24836.

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Therapeutic effect of high-frequency and low-frequency repetitive transcranial magnetic stimulation on delayed encephalopathy after acute carbon monoxide poisoning

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Therapeutic effect of high-frequency and low-frequency repetitive transcranial magnetic stimulation on delayed encephalopathy after acute carbon monoxide poisoning