• Food Science and Biotechnology
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• v.18 no.4
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• pp.923-927
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• 2009

This study is to investigate the anti-inflammatory effects of the ethylacetate extract of Rehmannia glutinosa (RGEAE). The anti-inflammatory activities using nitric oxide (NO), cytokine, and chemokine production in lipopolysaccharide (LPS)-induced RAW 264.7 cells were checked. Results indicated that RGEAE suppressed the NO, interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) production in a dose-dependent manner. Inhibition of NO formation was due to a decrease in inducible NOS (iNOS) expression. It was also found that the anti-inflammatory activities of RGEAE resulted from its inhibitory role on the nuclear factor $(NF)-{\kappa}B$ activation and reactive oxygen species (ROS) production. Therefore, it is suggested that RGEAE has potential as a therapeutic material to attenuate the inflammatory disease such as rheumatoid arthritis.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.1
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• pp.73-78
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• 2014

Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2 expression in Jurkat T cells, and this increased TCR-triggered AICD and enhanced TNFR gene expression. Also, knockdown of Bcl-2 in Jurkat T cells suppressed the gene expression of FLIP, TNF receptor-associated factors 3 (TRAF3) and TRAF4. Furthermore, suppressed Bcl-2 expression increased caspase-3 and diminished nuclear factor kappa B (NF-${\kappa}B$) translocation.

• KSBB Journal
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• v.28 no.6
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• pp.415-422
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• 2013

Gamma irradiation (${\gamma}IR$) is widely used for radiotherapy as a treatment of cancer cells although it has a risk to damage normal cells. Inflammation is regarded as one of side effects of ${\gamma}IR$ while the effect of low dose of ${\gamma}IR$ on inflammation has not been researched well. Here, we investigated the inflammatory responses of low dose of ${\gamma}IR$ on murine spleen cells. It was evaluated if ${\gamma}IR$ affected the mitogen-induced lymphocyte proliferation, the regulation of various inflammatory cytokines (IFN-${\gamma}$, IL-2, IL-17, IL-4, IL-10), and the involvement of Ikaros and MAPK/NF-${\kappa}B$ medicated mechanism. Exposure of $^{137}Cs-{\gamma}IR$ below 2 Gy decreased the lymphocytes proliferative response to mitogens (LPS, ConA) except at the lowest dose, 0.05 Gy. IL-17, IL-2 and IL-4 mRNA increased at 0.5 and 2 Gy, but not altered at 0.05 Gy. IL-10, anti-inflammatory cytokine, increased only at 0.05 Gy. In regard to intracellular signaling, p-JNK, p-p38 and p-$I{\kappa}B{\alpha}$ were not changed, whereas the activation of ERK and Ikaros increased at the lowest dose. These results suggest that exposure of ${\gamma}IR$ less than 0.5 Gy (or below 0.05 Gy) has beneficial effects as a radiation hormesis on immune function.

• Biomedical Science Letters
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• v.19 no.3
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• pp.173-179
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• 2013

Since the identification and characterization of toll-like receptors (TLR) in Drosophila, numerous scientific studies have examined the role of TLRs in host innate immunity. Recent studies have suggested a convergence of the nuclear factor kappa B (NF-${\kappa}B$) signaling and cytokine production regulated by the cytosolic elicitor known as NLRs (nucleotide-binding domain and leucine-rich repeat containing domain receptors) as a key modulator in inflammatory diseases. Among the NLRs, NOD1 and NOD2 have been intensively investigated for its role in inflammatory bowel disease (IBD). On the other hand, NLRs such as NLRP3, NLRP1, and NLRC4 (also known as IPAF) have been identified to form the inflammasome to activate downstream signaling molecules in response to pathogenic microbes. There is evidence to suggest that substantial crosstalk exists for the TLR and NLR signaling pathway in response to pathogen associated molecular pattern (PAMP). However, the substrate and the mechanistic role of NLRs are largely unknown in innate immune response. Understanding the signaling mechanisms by which NLRs recognize PAMP and other danger signals will shed light on elucidating the pathogenesis of various human inflammatory diseases such as IBD.

• BMB Reports
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• v.39 no.5
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• pp.479-491
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• 2006

Heme oxygenase (HO), the rate limiting enzyme in the breakdown of heme into carbon monoxide (CO), iron and bilirubin, has recently received overwhelming research attention. To date three mammalian HO isozymes have been identified, and the only inducible form is HO-1 while HO-2 and HO-3 are constitutively expressed. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-${\kappa}B$) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. The products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect against chemically-induced liver injury as well as hepatocarcinogenesis.

• Nutrition Research and Practice
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• v.8 no.1
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• pp.11-19
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• 2014

Synurus deltoides (Aiton) Nakai, belonging to the Compositae family, is an edible plant widely distributed in Northeast Asia. In this study, we examined the mechanisms underlying the immunomodulative effects of the ethanol extract of S. deltoides (SDE). The SDE extract strongly down-regulated the mRNA expression of the inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumour necrosis factor (TNF)-${\alpha}$, thereby inhibiting the production of nitric oxide (NO), prostaglandin E2 (PGE2), and TNF-${\alpha}$ in the lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Furthermore, SDE also suppressed the nuclear translocation of the activation protein (AP)-1 and the nuclear factor-${\kappa}B$ (NF-${\kappa}B$), and simultaneously decreased the phosphorylation of extracellular signal-regulated protein kinases (ERK), p38, and Akt. In agreement with the in vitro observations, the orally administered SDE ameliorated the acute inflammatory symptoms in the arachidonic acid-induced ear edema and the EtOH/HCl-induced gastritis in mice. Therefore, S. deltoides have a potential anti-inflammatory capacity in vitro and in vivo, suggesting the potential therapeutic use in the inflammation-associated disorders.

• CELLMED
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• v.7 no.4
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• pp.20.1-20.6
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• 2017

Inflammation has been linked to various diseases. Especially, fatigue is a frequent symptom in several inflammatory disorders. Therefore, blocking inflammatory process is effective in fatigue. We investigated whether Denmark porcine placenta (DPP) alleviates fatigue by inhibiting inflammatory reaction using forced swimming test (FST) animal model and RAW264.7 cells. In FST-induced fatigue animal model, the mice which received the DPP for 21 days showed decreases of interleukin $(IL)-1{\beta}$ and IL-6 serum levels. Furthermore, our data revealed that lipopolysaccharide (LPS)-induced $IL-1{\beta}$, IL-6, and tumor necrosis $factor-{\alpha}$ secretion were markedly inhibited by DPP in RAW264.7 cells without inducing cytotoxicity. LPS-enhanced nitric oxide secretion and inducible nitric oxide synthase expression were inhibited by DPP. The present study also figured out that these effects of DPP were mediated by blockade of caspase-1 and nuclear $factor-{\kappa}B$ activation. Taken together, our results indicated that DPP could be alleviating fatigue as candidate of anti-inflammatory agent.

• Biomedical Science Letters
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• v.19 no.4
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• pp.285-294
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• 2013

Chungyangeum (CYE) is a newly designed herbal drug formula for the purpose of treating atopic dermatitis. The aim of the present study is to elucidate whether and how CYE modulates the allergy inflammation in vitro and in vivo. We investigate to ascertain the pharmacological effects of CYE on both compound 48/80 or histamine-induced scratching behaviors and 2, 4-dinitrochlrobenzene (DNCB)-induced atopic dermatitis in mice. Additionally, we attempted to determine the effects of CYE on lipopolysaccharide (LPS)-induced inflammatory responses in macrophages. The findings of this study demonstrated that CYE reduced compound 48/80 or histamine-induced scratching behaviors and DNCB-induced atopic dermatitis in mice. The CYE inhibited the production of inflammatory cytokines as well as the activation of NF-${\kappa}B$ and caspase-1 in stimulated macrophages. Collectively, the findings of this study provide us with novel insights into the pharmacological actions of CYE as a potential molecule for use in the treatment of allergic inflammation diseases.

• Journal of Microbiology and Biotechnology
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• v.23 no.12
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• pp.1691-1698
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• 2013

The anti-inflammatory effects of Sargassum micracanthum ethanol extract (SMEE) was investigated using LPS-induced inflammatory response in this study. As a result, there was no cytotoxicity in the macrophage proliferation treated with SMEE compared with the control. SMEE inhibited production of nitric oxide and cytokines (IL-6, TNF-${\alpha}$, and IL-$1{\beta}$) in a dose-dependent manner. In addition, the expression of inducible nitric oxide synthase and cyclooxygenase 2 were suppressed via inhibition of nuclear factor ${\kappa}B$ p65 expression by SMEE treatment. The formation of edema in the mouse ear was reduced at the highest dose tested compared with that in the control, and reduction of ear thickness was observed in histological analysis. Moreover, in an acute toxicity test, no mortalities occurred in mice administered 5,000 mg/kg body weight of SMEE over a 2-week observation period. These results suggest that SMEE may have significant effects on inflammatory mediators and be a potential anti-inflammatory therapeutic material.

• Journal of Microbiology and Biotechnology
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• v.28 no.10
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• pp.1614-1625
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• 2018

Periodontitis, which is a severe inflammatory disease caused by endotoxins secreted from oral pathogens, destructs gingival tissue and alveolar bone. Curcuma xanthorrhiza, commonly called Java turmeric, has been shown to possess anti-bacterial and anti-inflammatory activities. The present study evaluated the inhibitory effect of C. xanthorrhiza supercritical extract (CXS) standardized with xanthorrhizol on lipopolysaccharide (LPS)-induced periodontitis in an animal model. LPS was topically injected into the periodontium of Sprague-Dawley rats to induce periodontitis and CXS (30 and $100mg{\cdot}kg^{-1}{\cdot}day^{-1}$) was orally administered after day 12. Histologically, CXS inhibited the collapse of gingival tissue by preventing cell infiltration. CXS significantly downregulated the expression of matrix metalloproteases (MMPs) and inflammation-related biomarkers, such as nuclear factor-kappa B ($NF-{\kappa}B$) and interleukin-1 beta ($IL-1{\beta}$) in gingival tissue. CXS also improved bone remodeling by downregulating osteoclastic transcription factors, such as nuclear factor of activated T-cells c1 (NFATc1), tartrate-resistant acid phosphatase (TRAP), and cathepsin K. In addition, CXS upregulated osteoblast differentiation-related markers, alkaline phosphate (ALP) and collagen type I alpha (COLA1). Thus, CXS can ameliorate periodontitis by inhibiting inflammation and improving bone remodeling.