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

Eom,Hye  Won; Park,Sun  Young; Kim,Young  Hun; Seong,Su  Jin; Jin,Mei  Ling; Ryu,Eun  Yeon; Kim,Min  Ju; Lee,Sang  Joon

doi:10.3892/ijmm.2012.1128

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

Authors:
- Hye Won Eom
- Sun Young Park
- Young Hun Kim
- Su Jin Seong
- Mei Ling Jin
- Eun Yeon Ryu
- Min Ju Kim
- Sang Joon Lee
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Affiliations: Department of Microbiology, Pusan National University, Busan, Republic of Korea, Bio-IT Fusion Technology Research Institute, Pusan National University, Busan, Republic of Korea
Published online on: September 18, 2012 https://doi.org/10.3892/ijmm.2012.1128
Pages: 1512-1520

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Abstract

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 Caulis 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-1 and nuclear erythroid-2 related factor 2 (Nrf-2) signaling pathways. We also reported that BCE inhibited lipopolysaccharide (LPS)-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-1 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.

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