Protective Effects of Arctium lappa L. Roots Against Hydrogen Peroxide-Induced Cell Injury and Potential Mechanisms in SH-SY5Y Cells

• Published in: Cellular and molecular neurobiology Vol. 35; no. 3; pp. 335 - 344
• Main Authors: Tian, Xing, Guo, Li-Ping, Hu, Xiao-Long, Huang, Jin, Fan, Yan-Hua, Ren, Tian-Shu, Zhao, Qing-Chun
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.04.2015
• Subjects: Antioxidants - isolation & purification; Antioxidants - pharmacology; Apoptosis - drug effects; Apoptosis - physiology; Arctium; Arctium lappa; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell Death - drug effects; Cell Death - physiology; Cell Line, Tumor; Cell Survival - drug effects; Cell Survival - physiology; Dose-Response Relationship, Drug; Humans; Hydrogen Peroxide - antagonists & inhibitors; Hydrogen Peroxide - toxicity; Neurobiology; Neurosciences; Original Research; Oxidative Stress - drug effects; Oxidative Stress - physiology; Plant Extracts - isolation & purification; Plant Extracts - pharmacology; Plant Roots; Protective Agents - isolation & purification; Protective Agents - pharmacology; Hydrogen peroxide; Neurodegenerative diseases; SH-SY5Y cells; ABTS
• ISSN: 0272-4340; 1573-6830
• DOI: 10.1007/s10571-014-0129-7

Accumulated evidence has shown that excessive reactive oxygen species (ROS) have been implicated in neuronal cell death related with various chronic neurodegenerative disorders. This study was designed to explore neuroprotective effects of ethyl acetate extract of Arctium lappa L. roots (EAL) on hydrogen peroxide (H 2 O 2 )-induced cell injury in human SH-SY5Y neuroblastoma cells. The cell viability was significantly decreased after exposure to 200 μM H 2 O 2 , whereas pretreatment with different concentrations of EAL attenuated the H 2 O 2 -induced cytotoxicity. Hoechst 33342 staining indicated that EAL reversed nuclear condensation in H 2 O 2 -treated cells. Meanwhile, TUNEL assay with DAPI staining showed that EAL attenuated apoptosis was induced by H 2 O 2 . Pretreatment with EAL also markedly elevated activities of antioxidant enzyme (GSH-Px and SOD), reduced lipid peroxidation (MDA) production, prevented ROS formation, and the decrease of mitochondrial membrane potential. In addition, EAL showed strong radical scavenging ability in 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) assays. Furthermore, EAL inhibited H 2 O 2 -induced apoptosis by increases in the Bcl-2/Bax ratio, decreases in cytochrome c release, and attenuation of caspase-3, caspase-9 activities, and expressions. These findings suggest that EAL may be regarded as a potential antioxidant agent and possess potent neuroprotective activity against H 2 O 2 -induced injury.