Bambusae Caulis in Taeniam modulates neuroprotective and anti-neuroinflammatory effects in hippocampal and microglial cells via HO-1-and Nrf-2-mediated pathways

被引:22
作者
Eom, Hye Won [1 ]
Park, Sun Young [2 ]
Kim, Young Hun [2 ]
Seong, Su Jin [1 ]
Jin, Mei Ling [1 ]
Ryu, Eun Yeon [2 ]
Kim, Min Ju [2 ]
Lee, Sang Joon [1 ]
机构
[1] Pusan Natl Univ, Dept Microbiol, Pusan 609735, South Korea
[2] Pusan Natl Univ, BioIT Fus Technol Res Inst, Pusan 609735, South Korea
基金
新加坡国家研究基金会;
关键词
microglial cells; hippocampal cells; heme oxygenase-1; nuclear erythroid-2 related factor 2; Bambusae Caulis in Taeniam; HEME OXYGENASE-1; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; ACTIVATION; INFLAMMATION; SYSTEM; BRAIN; CYTOKINES; INJURY; DAMAGE;
D O I
10.3892/ijmm.2012.1128
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Recent evidence indicates that microglial activation and hippocampal damage may play important roles in neurodegenerative diseases, including Alzheimer's disease. Bambusae Caulis in Taeniam has been used as a folk remedy for the treatment of hypertension and cardiovascular disease in China and Korea. In this study, the mechanism responsible for the neuroprotective and anti-neuroinflammatory effects of Bambusae Oxalis in Taeniam ethyl acetate fraction (BCE) was investigated. Heme oxygenase-1 (HO-1) is an inducible enzyme expressed in response to various inflammatory stimuli. Due to its role in the anti-inflammatory signaling pathway, the expression and modulation of HO-1 are important. In this study, the neuroprotective and anti-neuroinflammatory effects of BCE were examined using the murine microglial BV2 and hippocampal HT22 cells. We demonstrated that the administration of BCE provided neuroprotective effects against glutamate-induced cytotoxicity in HT22 cells through the HO-I and nuclear erythroid-2 related factor 2 (Nrf-2) signaling pathways. We also reported that BCE inhibited lipopolysaccharide (EPS)-induced pro-inflammatory cytokines and that the presence of selective inhibitors of HO-1 (SnPP) resulted in the inhibition of BCE-mediated anti-inflammatory activity in BV2 microglial cells. BCE was shown to induce HO-I expression as well as the nuclear translocation of Nrf-2 in both microglial and hippocampal cells. These findings revealed the potential therapeutic mechanisms of BCE in neurodegenerative diseases, suggesting that HO-1 and Nrf-2 signaling may play important roles in the mediation of its neuroprotective and anti-neuroinflammatory effects.
引用
收藏
页码:1512 / 1520
页数:9
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