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周围神经微电流刺激疗法对大脑中动脉闭塞大鼠模型的神经保护作用。

The Neuroprotective Effects of Peripheral Nerve Microcurrent Stimulation Therapy in a Rat Model of Middle Cerebral Artery Occlusion.

机构信息

Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan 31151, Republic of Korea.

Department of Medicine, College of Medicine, Keimyung University, Daegu 42601, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Sep 18;25(18):10034. doi: 10.3390/ijms251810034.


DOI:10.3390/ijms251810034
PMID:39337520
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11432279/
Abstract

This study investigated the neuroprotective effects of peripheral nerve microcurrent stimulation therapy in a rat model of middle cerebral artery occlusion (MCAO). Twenty 8-week-old male Sprague Dawley rats weighing 300-330 g were categorised into group A, serving as the healthy control; group B, including rats subjected to MCAO; group C, including rats receiving microcurrent therapy immediately after MCAO, which was continued for one week; and group D, including rats receiving microcurrent therapy one week before and one week after MCAO. A gross morphological analysis, behavioural motion analysis, histological examination, immunohistochemistry, and Western blotting were conducted. Microcurrent therapy significantly reduced ischaemic damage and pyramidal cells of the hippocampus CA1 region. Haematoxylin and eosin staining revealed infarction areas/viable pyramidal cell numbers of 0%/94.33, 28.53%/40.05, 17.32%/80.13, and 5.38%/91.34 in groups A, B, C, and D, respectively ( < 0.001). A behavioural analysis revealed that the total distances moved were 1945.24 cm, 767.85 cm, 1781.77 cm, and 2122.22 cm in groups A, B, C, and D, respectively ( < 0.05), and the mean speeds were 6.48 cm/s, 2.50 cm/s, 5.43 cm/s, and 6.82 cm/s, respectively ( < 0.05). Inflammatory markers (cluster of differentiation 68, interleukin-6, and tumour necrosis factor-α) significantly decreased in the treated groups ( < 0.001). Western blotting revealed reduced proinflammatory, oxidative stress, and apoptosis-related protein levels, along with increased angiogenic factors and mitogen-activated protein kinase (MAPK) pathway modulation in the treated groups. Peripheral nerve microcurrent stimulation therapy effectively mitigates ischaemic damage, promotes recovery, reduces inflammation, and modulates protein expression, emphasising its potential as a therapeutic strategy for ischaemic stroke.

摘要

本研究旨在探讨周围神经微电流刺激疗法对大脑中动脉闭塞(MCAO)大鼠模型的神经保护作用。将 20 只 8 周龄、体重 300-330g 的雄性 Sprague Dawley 大鼠分为 A 组(健康对照组)、B 组(MCAO 组)、C 组(MCAO 后立即接受微电流治疗,持续 1 周)和 D 组(MCAO 前和后各接受微电流治疗 1 周)。进行大体形态分析、行为运动分析、组织学检查、免疫组织化学和 Western blot 分析。微电流治疗显著减轻了缺血损伤和海马 CA1 区的锥体细胞。苏木精-伊红染色显示,A、B、C 和 D 组的梗死面积/存活锥体细胞数分别为 0%/94.33、28.53%/40.05、17.32%/80.13 和 5.38%/91.34(<0.001)。行为分析显示,A、B、C 和 D 组大鼠的总移动距离分别为 1945.24cm、767.85cm、1781.77cm 和 2122.22cm(<0.05),平均速度分别为 6.48cm/s、2.50cm/s、5.43cm/s 和 6.82cm/s(<0.05)。治疗组的炎症标志物(分化群 68、白细胞介素 6 和肿瘤坏死因子-α)显著降低(<0.001)。Western blot 分析显示,治疗组促炎、氧化应激和凋亡相关蛋白水平降低,同时促血管生成因子和丝裂原激活蛋白激酶(MAPK)通路调节因子水平升高。周围神经微电流刺激治疗可有效减轻缺血损伤,促进恢复,减轻炎症,调节蛋白表达,强调其作为缺血性脑卒中治疗策略的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/1e9428381726/ijms-25-10034-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/abb63cf50636/ijms-25-10034-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/60e0c773e73b/ijms-25-10034-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/3ba6b166540b/ijms-25-10034-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/9723a7849746/ijms-25-10034-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/2c3c91af9d43/ijms-25-10034-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/c9567c30314a/ijms-25-10034-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/cfa0b9d4dab5/ijms-25-10034-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/60b7358bd4f9/ijms-25-10034-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/1e9428381726/ijms-25-10034-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/abb63cf50636/ijms-25-10034-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/60e0c773e73b/ijms-25-10034-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/3ba6b166540b/ijms-25-10034-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/9723a7849746/ijms-25-10034-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/2c3c91af9d43/ijms-25-10034-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/c9567c30314a/ijms-25-10034-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/cfa0b9d4dab5/ijms-25-10034-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/60b7358bd4f9/ijms-25-10034-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5891/11432279/1e9428381726/ijms-25-10034-g009.jpg

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