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烟酰胺腺嘌呤二核苷酸磷酸氧化酶2的表达及α-硫辛酸对面神经损伤大鼠模型恢复的影响

Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Expression and Effects of Alpha Lipoic Acid on Recovery in a Rat Model of Facial Nerve Injury.

作者信息

Yoo Myung Chul, Ryu In Yong, Choi Jin Woo, Lee Jae Min, Byun Jae Yong, Yeo Seung Geun

机构信息

Department of Physical Medicine & Rehabilitation, College of Medicine, Kyung Hee University, Seoul 02447, Korea.

Department of Otorhinolaryngology, Head and Neck Surgery, College of Medicine, Kyung Hee University, Seoul 02447, Korea.

出版信息

Biomedicines. 2022 Jan 27;10(2):291. doi: 10.3390/biomedicines10020291.

DOI:10.3390/biomedicines10020291
PMID:35203501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8868592/
Abstract

BACKGROUND

NOX2 (nicotinamide adenine dinucleotide phosphate oxidase 2), which is upregulated by a variety of neurodegenerative factors, is neuroprotective and capable of reducing detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. The purpose of this study was to investigate NOX2 expression and the degree of functional recovery following different types of facial nerve injury and assess the effects of antioxidant intervention on nerve regeneration.

METHODS

A total of 40 mature (6-week-old) male Sprague-Dawley (SD) rats were used. After inducing facial injury (compression injury or cutting injury), we randomized rats into four groups: A, crushing injury only; B, crushing injury with alpha lipoic acid (ALA); C, axotomy only; and D, axotomy with ALA. Recovery from facial nerve injury was evaluated 4 and 14 days after injury by performing behavioral assessments (observational scale of vibrissae movement, modified scale of eye closing and blinking reflex) and measuring changes in NOX2 experimental/control ratio in the injured (left, experimental) facial nerve relative to that in the uninjured (right, control) facial nerve.

RESULTS

A comparison between groups according to the type of injury showed a higher NOX2 expression ratio in the axotomy group than in the crushing group ( < 0.001). Regardless of injury type, both groups that received an injection of ALA exhibited a trend toward a higher NOX2 expression ratio, although this difference reached statistical significance only in the axotomy group ( < 0.001). In behavioral assessments, overall behavioral test scores were significantly higher in the crushing injury group immediately after the injury compared with that in the axotomy group. Additionally, in behavioral tests conducted 4 days after the crushing injury, the group injected with ALA showed better results than the group without injection of ALA ( = 0.031).

CONCLUSIONS

Our study showed that NOX2 expression trended higher with facial nerve injury, exhibiting a significant increase with cutting-type injury. Furthermore, intraperitoneally injection with ALA may be an efficient strategy for accelerating peripheral facial nerve recovery after a crushing injury.

摘要

背景

烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NOX2)受多种神经退行性因子上调,具有神经保护作用,能够减轻缺血性和创伤性脑损伤以及慢性神经退行性疾病病理过程中的有害影响。本研究旨在调查不同类型面神经损伤后NOX2的表达及功能恢复程度,并评估抗氧化干预对神经再生的影响。

方法

共使用40只成熟(6周龄)雄性Sprague-Dawley(SD)大鼠。诱导面部损伤(压迫性损伤或切断性损伤)后,将大鼠随机分为四组:A组,仅压迫性损伤;B组,压迫性损伤并用α硫辛酸(ALA);C组,仅切断性损伤;D组,切断性损伤并用ALA。在损伤后4天和14天,通过进行行为评估(触须运动观察量表、改良闭眼和眨眼反射量表)以及测量损伤(左侧,实验组)面神经与未损伤(右侧,对照组)面神经中NOX2实验/对照比值的变化,来评估面神经损伤的恢复情况。

结果

根据损伤类型进行的组间比较显示,切断性损伤组的NOX2表达比值高于压迫性损伤组(<0.001)。无论损伤类型如何,接受ALA注射的两组均呈现出较高NOX2表达比值的趋势,尽管这种差异仅在切断性损伤组达到统计学意义(<0.001)。在行为评估中,损伤后即刻,压迫性损伤组的总体行为测试得分显著高于切断性损伤组。此外,在压迫性损伤后4天进行的行为测试中,注射ALA的组比未注射ALA的组结果更好(=0.031)。

结论

我们的研究表明,NOX2表达随面神经损伤而呈升高趋势,在切断性损伤时显著增加。此外,腹腔注射ALA可能是加速压迫性损伤后周围面神经恢复的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/091675671e1c/biomedicines-10-00291-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/829fd39a771d/biomedicines-10-00291-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/92ce76aa7024/biomedicines-10-00291-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/091675671e1c/biomedicines-10-00291-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/829fd39a771d/biomedicines-10-00291-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/92ce76aa7024/biomedicines-10-00291-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e1b5/8868592/091675671e1c/biomedicines-10-00291-g003.jpg

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