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水飞蓟素在脊髓损伤实验模型中的神经保护作用：通过调节 NF-κB/IκBα 通路。

Neuroprotective potential of fisetin in an experimental model of spinal cord injury: via modulation of NF-κB/IκBα pathway.

机构信息

Department of Neurosurgery.

Department of Pathology, Baoding First Central Hospital, Baoding, Hebei Province, China.

出版信息

Neuroreport. 2021 Mar 3;32(4):296-305. doi: 10.1097/WNR.0000000000001596.

DOI:10.1097/WNR.0000000000001596
PMID:33470764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7886366/
Abstract

AIM

To evaluate neuroprotective efficacy of fisetin against the experimental model of spinal cord injury (SCI).

MATERIALS AND METHODS

SCI was induced in male Sprague-Dawley rats by placing an aneurysm clip extradurally. Rats were treated either with vehicle or fisetin for 28 days after SCI.

RESULTS

Treatment with fisetin significantly attenuated SCI-induced alternations in mechano-tactile and thermal allodynia, hyperalgesia and nerve conduction velocities. SCI-induced upregulated tumor necrosis factor-alpha, interleukins, inducible nitric oxide synthase, cyclooxygenase-II, Bcl-2-associated X protein and caspase-3 mRNA expressions in the spinal cord and these were markedly reduced by fisetin. Spinal nuclear factor kappa B and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha protein levels were also significantly downregulated by fisetin. Hematoxylin and eosin staining of spinal cord suggested that fisetin significantly ameliorated histological aberrations such as neuronal degeneration, necrosis and inflammatory infiltration induced in it.

CONCLUSION

Fisetin exerts neuroprotection via modulation of nuclear factor kappa B/nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha pathway by inhibiting release of inflammatory mediators (inducible nitric oxide synthase and cyclooxygenase-II), proinflammatory cytokines (tumor necrosis factor-alpha and interleukins), apoptotic mediators (Bcl-2-associated X protein and caspase-3).

摘要

目的

评估非瑟酮对脊髓损伤（SCI）实验模型的神经保护作用。

材料和方法

通过硬膜外放置动脉瘤夹在雄性 Sprague-Dawley 大鼠中诱导 SCI。大鼠在 SCI 后 28 天用载体或非瑟酮治疗。

结果

非瑟酮治疗显著减轻了 SCI 引起的触觉和热痛觉过敏、痛觉过敏和神经传导速度的改变。SCI 诱导的脊髓肿瘤坏死因子-α、白细胞介素、诱导型一氧化氮合酶、环氧化酶-2、Bcl-2 相关 X 蛋白和半胱天冬酶-3 mRNA 表达上调，非瑟酮明显降低了这些表达。脊髓核因子 kappa B 和核因子 kappa 轻链增强子 B 细胞抑制剂-α蛋白水平也显著下调。非瑟酮明显改善了脊髓的组织学异常，如神经元变性、坏死和炎症浸润。

结论

非瑟酮通过抑制炎症介质（诱导型一氧化氮合酶和环氧化酶-2）、促炎细胞因子（肿瘤坏死因子-α和白细胞介素）、凋亡介质（Bcl-2 相关 X 蛋白和半胱天冬酶-3）的释放，通过调节核因子 kappa B/核因子 kappa 轻链增强子 B 细胞抑制剂-α通路发挥神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/f2ab2d62c225/nr-32-296-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/a354a57f575f/nr-32-296-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/1f0c64eeffc5/nr-32-296-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/7206e86d54b4/nr-32-296-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/f2ab2d62c225/nr-32-296-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/a354a57f575f/nr-32-296-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/1f0c64eeffc5/nr-32-296-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/7206e86d54b4/nr-32-296-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16c5/7886366/f2ab2d62c225/nr-32-296-g004.jpg

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