Cinnamaldehyde mitigates spinal cord injury in rats through anti-inflammatory and anti-apoptotic pathways.

IF 1.5 4区医学 Q3 CLINICAL NEUROLOGY

Neurological Research Pub Date : 2025-07-02 DOI:10.1080/01616412.2025.2520023

Hongming Zhang, Qing Han, Wendi Wang, Jian Liu, Qingbin Ni, Baoliang Sun, Guang Yin, Jingyi Sun

{"title":"Cinnamaldehyde mitigates spinal cord injury in rats through anti-inflammatory and anti-apoptotic pathways.","authors":"Hongming Zhang, Qing Han, Wendi Wang, Jian Liu, Qingbin Ni, Baoliang Sun, Guang Yin, Jingyi Sun","doi":"10.1080/01616412.2025.2520023","DOIUrl":null,"url":null,"abstract":"Background: Spinal cord injury (SCI) is a destructive neuropathological condition. Cinnamaldehyde (CA), a major bioactive component in Cinnamon essential oil, is known for its neuroprotective effects by inhibiting neuroinflammation, oxidative stress, and apoptosis. However, CA specific role in SCI remains unclear. The purpose of this study was to examine the impact of CA on SCI.Methods: We established a rat model of SCI and assessed nerve damage in rats using the Basso-Beattie-Bresnahan (BBB) locomotion scale, inclined plane test and Tarlov Scale. Neuronal loss was evaluated with Nissl and NeuN staining. Apoptotic damage was assessed using TUNEL staining and caspase3 analysis. The level of M1-type microglia activation was explored using Iba1. Additionally, TNF-α and IL-Iβ concentrations were measured to examine inflammation. Poly (ADP-ribose) polymerase (PARP) and proliferating cell nuclear antigen (PCNA) were used to assess DNA damage.Results: The results demonstrated that CA effectively improves behavioral scores measured by the BBB assay, inclined plane test, and Tarlov trial after SCI. NeuN and Nissl staining showed that CA significantly increases the number of NeuN-stained neurons and Nissl bodies. Apoptosis detection revealed that CA markedly reduces caspase3 production and the number of TUNEL-positive cells. Moreover, CA not only reduced Iba1 levels but also significantly decreased the production of TNF-α and IL-Iβ. Additionally, CA notably decreased PARP levels and promoted PCNA expression.Conclusions: CA regulates pathways involved in anti-neuroinflammation, anti-apoptosis, and DNA repair to improve neurological deficits and pathological conditions after SCI. CA therapeutic effect of CA may depend on the dosage.","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-13"},"PeriodicalIF":1.5000,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurological Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/01616412.2025.2520023","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Spinal cord injury (SCI) is a destructive neuropathological condition. Cinnamaldehyde (CA), a major bioactive component in Cinnamon essential oil, is known for its neuroprotective effects by inhibiting neuroinflammation, oxidative stress, and apoptosis. However, CA specific role in SCI remains unclear. The purpose of this study was to examine the impact of CA on SCI.

Methods: We established a rat model of SCI and assessed nerve damage in rats using the Basso-Beattie-Bresnahan (BBB) locomotion scale, inclined plane test and Tarlov Scale. Neuronal loss was evaluated with Nissl and NeuN staining. Apoptotic damage was assessed using TUNEL staining and caspase3 analysis. The level of M1-type microglia activation was explored using Iba1. Additionally, TNF-α and IL-Iβ concentrations were measured to examine inflammation. Poly (ADP-ribose) polymerase (PARP) and proliferating cell nuclear antigen (PCNA) were used to assess DNA damage.

Results: The results demonstrated that CA effectively improves behavioral scores measured by the BBB assay, inclined plane test, and Tarlov trial after SCI. NeuN and Nissl staining showed that CA significantly increases the number of NeuN-stained neurons and Nissl bodies. Apoptosis detection revealed that CA markedly reduces caspase3 production and the number of TUNEL-positive cells. Moreover, CA not only reduced Iba1 levels but also significantly decreased the production of TNF-α and IL-Iβ. Additionally, CA notably decreased PARP levels and promoted PCNA expression.

Conclusions: CA regulates pathways involved in anti-neuroinflammation, anti-apoptosis, and DNA repair to improve neurological deficits and pathological conditions after SCI. CA therapeutic effect of CA may depend on the dosage.

查看原文本刊更多论文

肉桂醛通过抗炎和抗凋亡途径减轻大鼠脊髓损伤。

背景：脊髓损伤（SCI）是一种破坏性的神经病理疾病。肉桂醛（CA）是肉桂精油中的主要生物活性成分，具有抑制神经炎症、氧化应激和细胞凋亡的神经保护作用。然而，CA在SCI中的具体作用尚不清楚。本研究的目的是探讨CA对脊髓损伤的影响。方法：建立脊髓损伤大鼠模型，采用BBB （Basso-Beattie-Bresnahan）运动量表、斜面测试和Tarlov量表评估大鼠神经损伤程度。Nissl和NeuN染色评估神经元损失。采用TUNEL染色和caspase3分析评估细胞凋亡损伤。用Iba1检测m1型小胶质细胞的激活水平。此外，测量TNF-α和il - i - β浓度以检查炎症。采用聚（adp -核糖）聚合酶（PARP）和增殖细胞核抗原（PCNA）评估DNA损伤。结果：结果表明，CA能有效改善脊髓损伤后BBB测定、斜面测试和Tarlov试验的行为评分。NeuN和Nissl染色显示，CA显著增加了NeuN染色的神经元和Nissl小体的数量。凋亡检测显示，CA显著降低caspase3的产生和tunel阳性细胞的数量。此外，CA不仅降低了Iba1水平，还显著降低了TNF-α和IL-Iβ的产生。此外，CA显著降低PARP水平，促进PCNA表达。结论：CA调节参与抗神经炎症、抗细胞凋亡和DNA修复的通路，改善脊髓损伤后的神经功能缺损和病理状况。CA的治疗效果可能取决于剂量。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Neurological Research 医学-临床神经学

CiteScore

3.60

自引率

0.00%

发文量

116

审稿时长

5.3 months

期刊介绍： Neurological Research is an international, peer-reviewed journal for reporting both basic and clinical research in the fields of neurosurgery, neurology, neuroengineering and neurosciences. It provides a medium for those who recognize the wider implications of their work and who wish to be informed of the relevant experience of others in related and more distant fields. The scope of the journal includes: •Stem cell applications •Molecular neuroscience •Neuropharmacology •Neuroradiology •Neurochemistry •Biomathematical models •Endovascular neurosurgery •Innovation in neurosurgery.