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水飞蓟宾载壳聚糖纳米粒对脑缺血再灌注损伤后海马 caspase-3 和 Bcl-2 表达的抗细胞凋亡作用。

Anti-apoptotic effect of silymarin-loaded chitosan nanoparticles on hippocampal caspase-3 and Bcl-2 expression following cerebral ischemia/reperfusion injury.

机构信息

Department of Biology, Faculty of Basic Sciences, University of Mazandaran, Babolsar, Iran.

Faculty of Biotechnology, Amol University of Special Modern Technologies, Amol, Iran.

出版信息

Int J Neurosci. 2022 Nov;132(11):1102-1109. doi: 10.1080/00207454.2020.1860971. Epub 2021 Jan 21.

DOI:10.1080/00207454.2020.1860971
PMID:33287594
Abstract

BACKGROUND

Cerebral ischemia/reperfusion (I/R) causes memory and learning impairments and apoptosis in the hippocampus. The aim of present study aimed to investigate the anti-apoptotic effects of silymarin-loaded chitosan nanoparticles (SM-CS-NPs) on the expression of Bcl-2 and Caspase-3 genes in hippocampal neurons after I/R injury.

MATERIAL AND METHODS

SM and SM-CS-NPs were orally administered (15 mg/kg) for 14 days, and then cerebral I/R injury was induced by the bilateral common carotid artery occlusion (BCCAO). One day after I/R induction, memory and learning impairments and various biochemical estimations were assessed.

RESULTS

Our results indicated that SM-CS-NPs improved I/R-induced memory and learning impairments and oxidative damage in the hippocampal region. The qRT-PCR analysis indicated that SM-CS-NPs pretreatment inhibited I/R-induced neuronal apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Caspase-3 in the hippocampus.

CONCLUSION

These findings suggest that SM-CS-NPs exert neuroprotective effects, and the neuroprotection is likely to be associated with the regulation of Bcl-2 and Caspase-3, leading to inhibition of apoptotic cell death in hippocampal neurons.

摘要

背景

脑缺血/再灌注(I/R)会导致海马区的记忆和学习损伤以及细胞凋亡。本研究旨在探讨水飞蓟素载壳聚糖纳米粒(SM-CS-NPs)对 I/R 损伤后海马神经元中 Bcl-2 和 Caspase-3 基因表达的抗凋亡作用。

材料与方法

SM 和 SM-CS-NPs 经口给药(15mg/kg)14 天,然后通过双侧颈总动脉闭塞(BCCAO)诱导脑 I/R 损伤。I/R 诱导后 1 天,评估记忆和学习损伤以及各种生化指标。

结果

我们的结果表明,SM-CS-NPs 改善了 I/R 诱导的记忆和学习损伤以及海马区的氧化损伤。qRT-PCR 分析表明,SM-CS-NPs 预处理通过增加 Bcl-2 的表达和降低 Caspase-3 的表达抑制了 I/R 诱导的神经元凋亡。

结论

这些发现表明 SM-CS-NPs 发挥了神经保护作用,这种神经保护可能与 Bcl-2 和 Caspase-3 的调节有关,从而抑制了海马神经元的细胞凋亡。

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