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姜黄素在血清/葡萄糖剥夺诱导的神经元 PC12 损伤模型中的疗效。

Curcumin Efficacy in a Serum/Glucose Deprivation-Induced Neuronal PC12 Injury Model.

机构信息

Medical Toxicology and Drug Abuse Research Center (MTDRC), Birjand University of Medical Sciences (BUMS), Birjand,Iran.

Faculty of Engineering and Natural Sciences, Sabanci University, Orta Mahalle, Üniversite Caddesi No. 27, Orhanlı, Tuzla, 34956 Istanbul,Turkey.

出版信息

Curr Mol Pharmacol. 2021;14(6):1146-1155. doi: 10.2174/1874467214666210203211312.

DOI:10.2174/1874467214666210203211312
PMID:33538682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8329120/
Abstract

BACKGROUND

Glucose/serum deprivation (GSD), has been used for understanding molecular mechanisms of neuronal damage during ischemia. It has been suggested that curcumin may improve neurodegenerative diseases.

AIM

In this study, the protective effects of curcumin and its underlying mechanisms were investigated in PC12 cells upon GSD-induced stress.

METHODS

PC12 cells were cultured in DMEM overnight and then incubated in GSD condition for either 6 or 12h. GSD-treated cells were pretreated with various concentrations of curcumin (10, 20, and 40 μM) for 5h. The cell viability, apoptosis, reactive oxygen species (ROS) level, oxidative stress, expression of apoptosis-related genes, and IL-6 were determined.

RESULTS

Curcumin increased cell viability and caused an anti-apoptotic effect in PC12 cells exposed for 12h to GSD . Curcumin also increased antioxidant enzyme expression, suppressed lipid peroxidation, and decreased interleukin-6 secretion in PC12 cells subjected to GSD. In addition, pretreatment with curcumin down-regulated pro-apoptotic (Bax), and up-regulated antiapoptotic (Bcl2) mediators.

CONCLUSION

Curcumin mitigates many of the adverse effects of ischemia, and therefore, should be considered as an adjunct therapy in ischemic patients.

摘要

背景

葡萄糖/血清剥夺(GSD)已被用于了解缺血期间神经元损伤的分子机制。有研究表明姜黄素可能改善神经退行性疾病。

目的

本研究旨在探讨姜黄素对 GSD 诱导的 PC12 细胞应激的保护作用及其潜在机制。

方法

PC12 细胞在 DMEM 中培养过夜,然后在 GSD 条件下孵育 6 或 12 小时。用不同浓度的姜黄素(10、20 和 40μM)预处理 GSD 处理的细胞 5 小时。测定细胞活力、凋亡、活性氧(ROS)水平、氧化应激、凋亡相关基因表达和白细胞介素 6。

结果

姜黄素增加了暴露于 GSD 12 小时的 PC12 细胞的细胞活力,并具有抗凋亡作用。姜黄素还增加了抗氧化酶的表达,抑制了 GSD 诱导的 PC12 细胞的脂质过氧化作用,并降低了白细胞介素 6 的分泌。此外,姜黄素预处理下调了促凋亡(Bax),上调了抗凋亡(Bcl2)介质。

结论

姜黄素减轻了缺血的许多不良影响,因此,应被视为缺血患者的辅助治疗。

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SOD2 Mediates Curcumin-Induced Protection against Oxygen-Glucose Deprivation/Reoxygenation Injury in HT22 Cells.超氧化物歧化酶2介导姜黄素对HT22细胞氧糖剥夺/复氧损伤的保护作用。
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