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地榆根通过调节 NADPH 氧化酶和 NF-E2 相关因子 2/血红素加氧酶-1 的表达来防止 6-羟多巴胺诱导的神经毒性。

Sanguisorbae radix protects against 6-hydroxydopamine-induced neurotoxicity by regulating NADPH oxidase and NF-E2-related factor-2/heme oxygenase-1 expressions.

机构信息

Department of Life and Nanopharmaceutical Science, College of Pharmacy and Kyung Hee East-West Pharmaceutical Research Institute, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.

出版信息

Phytother Res. 2013 Jul;27(7):1012-7. doi: 10.1002/ptr.4802. Epub 2012 Aug 30.

DOI:10.1002/ptr.4802
PMID:22933385
Abstract

6-Hydroxydopamine (6-OHDA) produces neuronal cell damage by generating reactive oxygen species (ROS). The major mechanisms of protection against ROS-induced stress are inhibiting expression of ROS generating genes such as NADPH oxidase (NOX) and increasing expression of endogenous antioxidant genes such as heme oxygenase-1 (HO-1). This study investigated whether a standardized Sanguisorbae Radix extract (SRE), a medical herb commonly used in Asian traditional medicine, has a protective effect on 6-OHDA-induced cell toxicity by regulating ROS in SH-SY5Y cells. SRE at 10 and 50 µg/mL significantly reduced 6-OHDA-induced cell damage dose dependently in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and by Hoechst 33342 staining. SRE increased the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X ratio and decreased cytochrome C release and caspase-3 activity. SRE also abolished 6-OHDA-induced ROS by inhibiting NOX expression and by inducing HO-1 expression via NF-E2-related factor-2 activation. Taken together, these results demonstrate that SRE has protective effects against 6-OHDA-induced cell death by regulating ROS in SH-SY5Y cells.

摘要

6-羟多巴胺(6-OHDA)通过产生活性氧物种(ROS)导致神经元细胞损伤。抵抗 ROS 诱导应激的主要机制是抑制 ROS 生成基因如 NADPH 氧化酶(NOX)的表达和增加内源性抗氧化基因如血红素加氧酶-1(HO-1)的表达。本研究通过调节 SH-SY5Y 细胞中的 ROS,探讨了一种常用的亚洲传统医学药用植物地榆提取物(SRE)是否对 6-OHDA 诱导的细胞毒性具有保护作用。SRE 在 10 和 50μg/mL 时通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)分析和 Hoechst 33342 染色显著地剂量依赖性降低了 6-OHDA 诱导的细胞损伤。SRE 通过增加 B 细胞淋巴瘤 2(Bcl-2)/Bcl-2 相关 X 比值并减少细胞色素 C 释放和半胱天冬酶-3 活性来增加细胞活力。SRE 还通过抑制 NOX 表达和通过 NF-E2 相关因子-2 激活诱导 HO-1 表达来消除 6-OHDA 诱导的 ROS。总之,这些结果表明 SRE 通过调节 SH-SY5Y 细胞中的 ROS 对 6-OHDA 诱导的细胞死亡具有保护作用。

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