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白藜芦醇对甲卡西酮诱导的小鼠中脑多巴胺能神经元神经毒性的神经保护作用。

Neuroprotection of resveratrol against neurotoxicity induced by methamphetamine in mouse mesencephalic dopaminergic neurons.

机构信息

Key Laboratory for Experimental Teratology of the Ministry of Education and Department of Anatomy, Shandong University, School of Medicine, Jinan, Shandong, China.

Department of Radiology, The second Hoppital of Shandong University, Jinan, Shandong, China.

出版信息

Biofactors. 2015 Jul-Aug;41(4):252-60. doi: 10.1002/biof.1221. Epub 2015 Jul 24.

DOI:10.1002/biof.1221
PMID:26212417
Abstract

Resveratrol is originally extracted from huzhang, a Chinese herbal medicine. Recently, resveratrol has attracted a great of attention due to its antioxidant and antiapoptotic properties. Although the neuroprotection of resveratrol on neural damages in various models has been well characterized, little is known about the role of resveratrol in methamphetamine (MA) induced neurotoxicity in mesencephalic dopaminergic neurons. Dopaminergic neurons were isolated from midbrain of mouse embryos at embryonic day 15 and cultured in the presence of MA and resveratrol. Cell viability was examined by MTT assay and the apoptosis was assessed using Hoechst33342/PI double staining. To evaluate the Oxidative damage, ROS assay was performed. Moreover, the changes of time course of intracellular free calcium concentration ([Ca(2+) ]i) were analyzed with Fluo-3/AM tracing. The data showed that MA induced the neurotoxicity of cultured cells in a dose-dependent manner. Resveratrol significantly increased cellular viability and retarded cell apoptosis. Furthermore, resveratrol also attenuated MA induced ROS production and intracellular free calcium overload. Our results suggest that resveratrol protects dopaminergic neurons from MA-induced neuronal cytotoxicity, which, at least partly, is mediated by inhibition of [Ca(2+) ]i and oxidative stress. © 2015 BioFactors 41(4):252-260, 2015.

摘要

白藜芦醇最初是从中国草药虎杖中提取的。最近,由于其抗氧化和抗细胞凋亡特性,白藜芦醇引起了广泛关注。虽然白藜芦醇在各种模型中对神经损伤的神经保护作用已得到很好的描述,但对于白藜芦醇在中脑中多巴胺能神经元中甲氧麻(MA)诱导的神经毒性中的作用知之甚少。多巴胺能神经元是从胚胎 15 天的胎鼠中脑分离出来的,并在 MA 和白藜芦醇的存在下进行培养。通过 MTT 测定法检查细胞活力,并通过 Hoechst33342/PI 双重染色评估细胞凋亡。为了评估氧化损伤,进行了 ROS 测定。此外,通过 Fluo-3/AM 示踪分析了细胞内游离钙浓度 ([Ca(2+) ]i) 的时程变化。数据表明,MA 以剂量依赖的方式诱导培养细胞的神经毒性。白藜芦醇显著增加细胞活力并延缓细胞凋亡。此外,白藜芦醇还减轻了 MA 诱导的 ROS 产生和细胞内游离钙超载。我们的结果表明,白藜芦醇可保护多巴胺能神经元免受 MA 诱导的神经元细胞毒性,这至少部分是通过抑制 [Ca(2+) ]i 和氧化应激来介导的。©2015 BioFactors 41(4):252-260, 2015.

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