title: Acanthopanax senticosus exerts neuroprotective effects through HO-1 signaling in hippocampal and microglial cells.
abstract: Extracts of Acanthopanax senticosus, a traditional herb commonly found in Northeastern Asia, are used for treating neurodegenerative disorders such as ischemia and depression. However, the mechanisms of its neuroinflammatory and cytoprotective effects have not been investigated. We examined the mechanism of A. senticosus activity in anti-neuroinflammatory and neuroprotective processes. HO-1 is an inducible enzyme present in most cell lines. ASE increased HO-1 expression, which reduced LPS-induced nitric oxide/ROS production in BV2 cells. Moreover, the induction of HO-1 expression protected cells against glutamate-induced neuronal cell death. Activation of the p38-CREB pathway and translocation of Nrf2 are strongly involved in ASE-induced HO-1 expression. Our results showed that ASE-induced HO-1 expression through the p38-CREB pathway plays an important role in the generation of anti-neuroinflammatory and neuroprotective responses. ASE also increases the translocation of Nrf2 to regulate HO-1 expression. Furthermore, our results indicate that ASE serves as a potential therapeutic agent for neuronal disorders.
authors: Department of Microbiology, Pusan National University, Busan 609-735, Republic of Korea.
authors: Mei Ling
authors: ML
authors: Jin
authors: Sun Young
authors: SY
authors: Park
authors: Young Hun
authors: YH
authors: Kim
authors: Geuntae
authors: G
authors: Park
authors: Sang Joon
authors: SJ
authors: Lee
mesh_terms: D000818:Animals; D016923:Cell Death / Q000187:drug effects; D002460:Cell Line / Q000187:drug effects; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D028001:Eleutherococcus / Q000737:chemistry*; D018698:Glutamic Acid / Q000009:adverse effects; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008565:Membrane Proteins / Q000378:metabolism*; D051379:Mice; D017628:Microglia / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D020258:Neurotoxicity Syndromes / Q000188:drug therapy / Q000209:etiology; D009569:Nitric Oxide / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology*; D010946:Plants, Medicinal / Q000737:chemistry; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: C492004:Creb1 protein, mouse; D017362:Cyclic AMP Response Element-Binding Protein; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D051267:NF-E2-Related Factor 2; D018696:Neuroprotective Agents; C495636:Nfe2l2 protein, mouse; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D018698:Glutamic Acid; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse