title: Sanguisorbae radix protects against 6-hydroxydopamine-induced neurotoxicity by regulating NADPH oxidase and NF-E2-related factor-2/heme oxygenase-1 expressions.
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.
authors.affiliation: 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.
authors.forename: Hyein
authors.initials: H
authors.lastname: Oh
authors.forename: Jinyoung
authors.initials: J
authors.lastname: Hur
authors.forename: Gunhyuk
authors.initials: G
authors.lastname: Park
authors.forename: Hyo Geun
authors.initials: HG
authors.lastname: Kim
authors.forename: Young Ock
authors.initials: YO
authors.lastname: Kim
authors.forename: Myung Sook
authors.initials: MS
authors.lastname: Oh
mesh_terms: D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D053148:Caspase 3 / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000096:biosynthesis; D059290:Dopaminergic Neurons / Q000187:drug effects; D019254:Genes, bcl-2 / Q000502:physiology; D051547:Heme Oxygenase-1 / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D019255:NADPH Oxidases / Q000096:biosynthesis / Q000235:genetics; D051267:NF-E2-Related Factor 2 / Q000096:biosynthesis / Q000235:genetics; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D016627:Oxidopamine / Q000037:antagonists & inhibitors; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use*; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors* / Q000378:metabolism; D031993:Sanguisorba / Q000737:chemistry*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; D051267:NF-E2-Related Factor 2; D018696:Neuroprotective Agents; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D016627:Oxidopamine; D045304:Cytochromes c; D051547:Heme Oxygenase-1; D019255:NADPH Oxidases; D053148:Caspase 3