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黄芩素拮抗鱼藤酮诱导的帕金森病相关多巴胺能 SH-SY5Y 细胞凋亡。

Baicalein antagonizes rotenone-induced apoptosis in dopaminergic SH-SY5Y cells related to Parkinsonism.

机构信息

School of Chinese Medicine, The University of Hong Kong, 10 Sassoon Road, Pokfulam, Hong Kong SAR, China.

出版信息

Chin Med. 2012 Jan 21;7(1):1. doi: 10.1186/1749-8546-7-1.

Abstract

BACKGROUND

Two active compounds, baicalein and its glycoside baicalin were found in the dried root of Scutellaria baicalensis Georgi, and reported to be neuroprotective in vitro and in vivo. This study aims to evaluate the protective effects of baicalein on the rotenone-induced apoptosis in dopaminergic SH-SY5Y cells related to parkinsonism.

METHODS

Cell viability and cytotoxicity were determined by MTT assay. The degree of nuclear apoptosis was evaluated with a fluorescent DNA-binding probe Hoechst 33258. The production of reactive oxidative species (ROS) and loss of mitochondrial membrane potential (ΔΨm) were determined by fluorescent staining with DCFH-DA and Rhodanmine 123, respectively. The expression of Bax, Bcl-2, cleaved caspase-3 and phosphorylated ERK1/2 was determined by the Western blots.

RESULTS

Baicalein significantly increased viability and decreased rotenone-induced death of SH-SY5Y cells in a dose-dependent manner. Pre- and subsequent co-treatment with baicalein preserved the cell morphology and attenuated the nuclear apoptotic characteristics triggered by rotenone. Baicalein antagonized rotenone-induced overproduction of ROS, loss of ΔΨm, the increased expression of Bax, cleaved caspase-3 and phosphorylated ERK1/2 and the decreased expression of Bcl-2.

CONCLUSION

The antioxidative effect, mitochondrial protection and modulation of anti-and pro-apoptotic proteins are related to the neuroprotective effects of baicalein against rotenone induced cell death in SH-SY5Y cells.

摘要

背景

黄芩的干燥根中发现了两种活性化合物,黄芩素和其糖苷黄芩苷,并且已在体外和体内证实具有神经保护作用。本研究旨在评估黄芩素对与帕金森病相关的鱼藤酮诱导的多巴胺能 SH-SY5Y 细胞凋亡的保护作用。

方法

通过 MTT 测定法测定细胞活力和细胞毒性。用荧光 DNA 结合探针 Hoechst 33258 评估核凋亡程度。通过用 DCFH-DA 和罗丹明 123 荧光染色分别测定活性氧物种 (ROS)的产生和线粒体膜电位 (ΔΨm) 的损失。通过 Western blot 测定 Bax、Bcl-2、裂解的 caspase-3 和磷酸化 ERK1/2 的表达。

结果

黄芩素呈剂量依赖性显著增加 SH-SY5Y 细胞的活力并降低鱼藤酮诱导的死亡。黄芩素的预处理和后续共同处理可维持细胞形态并减轻鱼藤酮引发的核凋亡特征。黄芩素拮抗鱼藤酮诱导的 ROS 过度产生、ΔΨm 损失、Bax、裂解的 caspase-3 和磷酸化 ERK1/2 的表达增加以及 Bcl-2 的表达减少。

结论

抗氧化作用、线粒体保护和抗凋亡蛋白与黄芩素对鱼藤酮诱导的 SH-SY5Y 细胞死亡的神经保护作用有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/404e/3275529/ce481851ddaf/1749-8546-7-1-1.jpg

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