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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.
International Journal of Molecular Medicine 09/2012; · 1.98 Impact Factor
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ABSTRACT: Acanthopanax senticosus (Rupr. & Maxim.) Harms (AS) has been used as a traditional medicine for the treatment of hypertension, rheumatism, ischemic heart disease, diabetes, and hepatitis in East Asia. This herb has been reported to possess anti-cancer, anti-diabetes, and anti-inflammatory properties.
To examine the anti-inflammatory activity of AS extract (ASE) and its mechanism of action in Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS)-stimulated macrophages.
P. gingivalis LPS was used to induce an inflammatory response in the murine macrophage cell line RAW 264.7. Pro-inflammatory cytokines were measured by using an enzyme-linked immunosorbent assay. We used western blot assays and real-time quantitative polymerase chain reaction to detect protein and mRNA expression, respectively. Luciferase assays were performed to determine the transactivity of transcription factors. Nuclear translocation of nuclear factor (NF)-κB was assessed by confocal microscopy.
ASE significantly induced the expression and activity of heme oxygenase-1 (HO-1), which is known to produce an anti-inflammatory effect, in RAW 264.7 cells, through NF-E2-related factor 2 (Nrf-2), Janus kinase, and extracellular signal-regulated kinase activation. ASE also effectively suppressed the production of pro-inflammatory cytokines, tumor necrosis factor α, interleukin (IL)-1β, and IL-6, and decreased the nuclear translocation and transactivity of activator protein-1 (AP-1) and NF-κB by inhibiting the phosphorylation of IκB-α in P. gingivalis LPS-stimulated macrophage cells. Furthermore, ASE inhibits signal transducer and activator of transcription (STAT)1 phosphorylation while it activates STAT3 phosphorylation in P. gingivalis LPS-stimulated RAW 264.7 cells.
Our study suggests that ASE produces anti-inflammatory effects on P. gingivalis LPS-stimulated macrophages through a reduction in AP-1 and NF-κB activity, modulation of STAT1 and STAT3 phosphorylation, and upregulation of HO-1 expression through the activation of mitogen-activated protein kinase and Nrf-2 signaling pathways. Therefore, ASE could be a candidate for the prevention and treatment of periodontal diseases that involve excessive inflammation.
Journal of ethnopharmacology 06/2012; 142(3):819-28. · 2.32 Impact Factor
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ABSTRACT: Recently, it has been reported that several natural extracts have anti-inflammatory effects through HO-1 induction. In this study, we used the ethyl acetate fraction of Bambusae Caulis in Taeniam (BCE) to investigate its anti-inflammatory effect on macrophages stimulated with LPS from Porphyromonas gingivalis. BCE inhibited the production of pro-inflammatory cytokines in P. gingivalis LPS-stimulated RAW264.7 cells. BCE also suppressed the nuclear translocation of NF-κB and AP-1. A selective inhibitor of HO-1 attenuated BCE's inhibitory effects on the production of pro-inflammatory cytokines. BCE also dose-dependently increased HO-1 expression at both the mRNA and the protein levels. BCE increased nuclear translocation of Nrf-2. Finally, a specific inhibitor of p38 reduced BCE-induced HO-1 expression and BCE-induced phosphorylation of p38 MAPK. BCE induced anti-inflammatory effects by activating Nrf-2-mediated HO-1 induction via p38 signaling in P. gingivalis LPS-stimulated macrophages. This result indicates that BCE is a promising therapeutic agent for combating periodontitis.
Environmental toxicology and pharmacology. 05/2012; 34(2):315-323.
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ABSTRACT: Periodontitis is an oral chronic inflammatory disease that influences systemic diseases. Heme oxygenase-1 has several beneficial abilities through Nrf-2 regulation. Ginkgo biloba has been reported to have anti-inflammatory effects associated with heme oxygenase-1 (HO-1) expression. In this study, we investigated whether the anti-inflammatory effects of G. biloba were involved with Nrf-2-mediated HO-1 expression in Porphyromonas gingivalis LPS-stimulated RAW264.7 macrophage cells. G. biloba was extracted with ethyl acetate (EGB). EGB exhibited anti-inflammatory activities, which suppressed the production of pro-inflammatory mediators, the activation of mitogen-activated protein kinases, and nuclear translocation of transcription factors. EGB also up-regulated the HO-1 expression, and the Nrf-2 level in the nucleus and its transactivity. Furthermore, reduced pro-inflammatory mediator levels by EGB were inverted in the presence of SnPP. The collective results suggest that the anti-inflammatory effects of EGB are due to the HO-1 expression via up-regulation of Nrf-2 in RAW 264.7 cells stimulated by P. gingivalis LPS.
Inflammation 04/2012; 35(4):1477-86. · 1.75 Impact Factor
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ABSTRACT: Periodontitis, a chronic inflammatory periodontal disease that develops from gingivitis, is caused by periodontal pathogenic bacteria such as Porphyromonas gingivalis. Recent studies have focused on the antioxidant, anti-human immunodeficiency virus, anticarcinogenic, and anti-inflammatory properties of gomisins. However, the anti-inflammatory activities of gomisin plants through heme oxygenase-1 (HO-1) signals remain poorly defined. We found that gomisins' anti-inflammatory activity occurs via the induction of HO-1 expression. Gomisins G and J inhibit the production of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 and also block nuclear factor-κB activation in Raw264.7 cells stimulated with P. gingivalis lipopolysaccharide. Furthermore, pro-inflammatory cytokine production is inhibited through the induction of HO-1 expression. HO-1 expression is induced by all gomisins, but their anti-inflammatory activity via HO-1 signaling is observed with gomisins G and J, and not A. We found that gomisins G and J extracted from Schisandria chinensis can inhibit the P. gingivalis lipopolysaccharide induced-inflammatory responses in Raw264.7 cells.
Journal of medicinal food 12/2011; 14(12):1519-26. · 1.39 Impact Factor
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ABSTRACT: Microbial fuel cells (MFCs) were successfully enriched using sludge contaminated with Cr(VI) and their characteristics were investigated. After enrichment, the charge of the final 10 peaks was 0.51 C +/- 1.16%, and the anodic electrode was found to be covered with a biofilm. The enriched MFCs removed 93% of 5 mg/l Cr(VI) and 61% of 25 mg/l Cr(VI). 16S rDNA DGGE profiles from the anodic electrode indicated that beta-Proteobacteria, Actinobacteria, and Acinetobacter sp. dominated. This study is the first to report that electrochemically active and Cr(VI)-reducing bacteria could be enriched in the anode compartment of MFCs using Cr(VI)-containing sludge and demonstrates the Cr(VI) removal capability of such MFCs.
Journal of Microbiology and Biotechnology 02/2011; 21(2):187-91. · 1.38 Impact Factor
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ABSTRACT: Porphyromonas gingivalis is considered the major pathogen of periodontal disease, which leads to chronic inflammation in oral tissues. P. gingivalis-produced lipopolysaccharide (LPS) is a key factor in the development of periodontitis. It is established that surfactin produced by Bacillus subtilis confers anti-inflammatory properties. However, the underlying mechanisms responsible for surfactin-induced anti-inflammatory actions in the context of periodontitis are poorly understood. In this study, we investigated whether surfactin affected P. gingivalis LPS-induced pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-12, and determined that it significantly inhibited their production. Surfactin-mediated inhibition was mainly due to blocked activation of P. gingivalis LPS-triggered nuclear factor-κB. We also examined whether the regulatory effect of surfactin on P. gingivalis LPS-stimulated human THP-1 macrophages was mediated by the induction of heme oxygenase-1 (HO-1) signals, and determined that surfactin also induced HO-1 mRNA and protein expression via activation of Nrf-2. Additionally, we found that small interfering RNA-mediated knock-down of Nrf-2 significantly inhibited surfactin-induced HO-1 expression. Furthermore, inhibition of phosphoinositide 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) significantly decreased surfactin-induced HO-1 expression, which is consistent with the suggestion that surfactin-induced HO-1 expression occurs via PI3K/Akt, ERK, and Nrf-2. Treatment with a selective inhibitor of HO-1 reversed the surfactin-mediated inhibition of pro-inflammatory cytokines, suggesting that surfactin induces anti-inflammatory effects by activating Nrf-2-mediated HO-1 induction via PI3K/Akt and ERK signaling. Collectively, these observations support the potential of surfactin as a candidate in strategies to prevent caries, periodontitis, or other inflammatory diseases.
Chemico-biological interactions 12/2010; 188(3):437-45. · 2.46 Impact Factor
