• Advances in Traditional Medicine
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• v.8 no.1
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• pp.1-16
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• 2008

Immunity is responsible for the defense mechanism of the body but in case of autoimmune diseases, its role gets diverted. Like so many other diseases, asthma is also considered as one of the most common autoimmune diseases to be occurring in community. Asthma is defined as a chronic inflammatory airway disease that is characterized by airway hyper reactivity and mucus hypersecretion that result in intermittent airway obstruction. The incidence of allergic asthma has almost doubled in the past two decades. Although, precise causative mechanism of asthma is unknown, but several mechanisms have been proposed that is immunological, pharmacological and genetic mechanisms, and airway and neurogenic inflammation. The inflammatory process observed in the asthmatic patients is the final result of a complex network of interactions between various immunological cell lineages, its mediators and secreted substances. Thus, among the mechanisms proposed, the immunological one plays a key role. Through this article, we have tried to provide some insight into immunological mechanisms in pathogenesis of asthma.

• YAKHAK HOEJI
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• v.47 no.2
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• pp.69-77
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• 2003

Arachidonic acid (AA), which is stored in membrane glycerophospholipids, is liberated by phospholipase $A_2$ (PLA$_2$) enzymes and is sequentially converted to cyclooxygenases (COXs) and lipoxygenases (LOXs) then to various bioactive PGs, and LTs. In order to find the specific inhibitors of AA metabolism especially PLA$_2$, COX-2, 5-LO and lyso PAF acetyltransferase, 120 Korean residential plants extracts were evaluated for their inhibitory activity on PGD$_2$, LTC$_4$ production from cytokine-induced mouse bone marrow-derived mast cells (BMMC) and arachidonic acid released from phospholipid and PAF production from lyso PAF. From this screening procedure, methanol extract of ten indigenous plant such as Salix gracilistyla, Sedum kamtschaticum, Cirsium chanroenicum, Hypericum ascyron, Astilbe chinensis, Agrimonia pilosa, Aristolochia manshuriensis, Vodia daniellii, Pyrola japonica, Styrax obassia were found to inhibit production of inflammatory mediators in vitro assay system.

• Food Science and Biotechnology
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• v.18 no.3
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• pp.813-817
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• 2009

The effect of 4 seaweed extracts (Desmarestia viridis, Dictyopteris divaricata, Scytosiphon lomentaria, and Ishige okamurae) on pro-inflammatory mediators as well as nuclear factor $(NF)-{\kappa}B$ in the stimulated Raw 264.7 cells was investigated. They reduced iNOS and interlukin $(IL)-1{\beta}$ expressions at transcription level. Of those, 3 extracts (D. divaricata, I. okamurae, and S. lomentaria) inhibited the COX-2 expression at translation level. $I{\kappa}B-{\alpha}$ degradation was inhibited by D. divaricata and S. lomentaria extracts. Therefore, we concluded that the extracts from D. divaricata and S. lomentaria could inhibit the activation of murine macrophage through the blocking of $NF-{\kappa}B$ activation.

• Biomedical Science Letters
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• v.24 no.4
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• pp.398-404
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• 2018

To evaluate the antioxidant and anti-neuroinflammatory effects of defatted Perilla frutescens extract (DPE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Cell viabilities were estimated by MTT assay. LPS-stimulated BV-2 microglia were used to study the expression and production of inflammatory mediators such as nitric oxide (NO), inducible NO synthase (iNOS), Cyclooxygenase-2 (COX-2), and prostaglandin $E_2$ ($PGE_2$). Pretreatment with DPE prior to LPS treatment significantly inhibited excessive production of NO (10, 25, 50, 75, and $100{\mu}g/mL$) in a dose-dependent manner, and was associated with down regulation of expression of iNOS and COX-2. DPE also suppressed the LPS-induced increase in $PGE_2$ level (10, 25, 50, 75, and $100{\mu}g/mL$) in BV-2 cells. Therefore, DPE can be considered as a useful therapeutic and preventive approach for the treatment of several neurodegenerative diseases.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.378.1-378.1
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• 2002

Prostaglandins (PGs) and nitric oxide (NO) are essential to maintain homeostasis and defensa systems in human beings. However. overproduced PGs and NO by inducible cyclooxygenase (COX-2) and inducible nitric oxide synthase (iNOS), respectively. cause tissue damages. chronic inflammation. and carcinogenesis. In this view. the potential COX-2 or iNOS inhibitors have been considered as anti-inflammatory or cancer chemopreventive agents. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.145.1-145.1
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• 2003

Several lines of recent evidences have shown that several pro-inflammatory genes or mediators, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 and cytokines (e.g., tumor necrosis factor $\alpha$ and interleukin-1$\beta$), are strongly expressed in the ischemic brain. Inflammation is now recognized as a significant contributing mechanism in cerebral ischemia because anti-inflammatory compounds or inhibitors of iNOS and cyclooxygenase-2 have been proven to reduce ischemic brain damage. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.205.1-205.1
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• 2003

Several lines of recent evidences have shown that several pro-inflammatory genes or mediators, such as inducible nitric oxide synthase (iNOS)are strongly expressed in the ischemic brain. Inflammation is now recognized as a significant contributing mechanism in cerebral ischemia because anti-inflammatory compounds or inhibitors of iNOS have been proven to reduce ischemic brain damage. In iNOS assay, hexane fraction of M61 inhibited NO (iNOS IC50, 0.7${\mu}$g/ml). In vivo study was carried out to evaluate neuroprotective effect of hexane fraction of M61 after transient global ischemia using Mongolian gerbil ischemia model. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.260.1-260.1
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• 2002

Green tea contains several antioxidants including polyphenols of the catechin. which have been shown to act in vitro and in vivo as anti-inflammatory. anti-viral and anti-tumor drugs. Prostaglandins (PGs) are a family of intercellular and intracellular messengers derived from arachidonic acid(AA) by phospholipase(PL) and cyclooxygenase(COX). These mediators exert a wide range of effects on processes such as smooth muscle tone. vascular permeability, cellular proliferation. and inflammatory/immune function. (omitted)

• Biomolecules & Therapeutics
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• v.18 no.2
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• pp.135-144
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• 2010

The pro-oxidative and pro-inflammatory pathways in vascular endothelium have been implicated in the initiation and progression of atherosclerosis. In fact, inflammatory responses in vascular endothelium are primarily regulated through oxidative stress-mediated signaling pathways leading to overexpression of pro-inflammatory mediators. Enhanced expression of cytokines, chemokines and adhesion molecules in endothelial cells and their close interactions facilitate recruiting and adhering blood leukocytes to vessel wall, and subsequently stimulate transendothelial migration, which are thought to be critical early pathologic events in atherogenesis. Although interleukin-4 (IL-4) was traditionally considered as an anti-inflammatory cytokine, recent in vitro and in vivo studies have provided robust evidence that IL-4 exerts pro-inflammatory effects on vascular endothelium and may play a critical role in the development of atherosclerosis. The cellular and molecular mechanisms responsible for IL-4-induced atherosclerosis, however, remain largely unknown. The present review focuses on the distinct sources of IL-4-mediated reactive oxygen species (ROS) generation as well as the pivotal role of ROS in IL-4-induced vascular inflammation. These studies will provide novel insights into a clear delineation of the oxidative mechanisms of IL-4-mediated stimulation of vascular inflammation and subsequent development of atherosclerosis. It will also contribute to novel therapeutic approaches for atherosclerosis specifically targeted against pro-oxidative and pro-inflammatory pathways in vascular endothelium.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.6
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• pp.1032-1038
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• 2011

Yeonguemjiri-tang(連芩止痢湯, YGT) exhibits potent anti-inflammatory activity in widely intestine disease, but its mechanism undisclosed. To elucidate the molecular mechanisms of YGT on pharmacological and biochemical actions in inflammation, we examined the effect of YGT on pro-inflammatory mediators in phorbol 12-myristate 13-acetate (PMA) plus A23187-induced mast cell and lipopolysaccharide (LPS)-stimulated macrophages. The investigation focused on whether YGT inhibited pro-inflammatory cytokines such as interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in PMA plus A23187-induced HMC-1 cells and inflammatory madiators such as nitric oxide (NO), TNF-${\alpha}$, IL-6, iNOS, COX-2 in LPS-stimulated RAW 264.7 cells. We found that YGT inhibited LPS-induced NO, TNF-${\alpha}$ and IL-6 productions as well as the expressions of iNOS and COX-2. These results suggest that YGT has inhibitory effects on mast cell-mediated and macrophage-mediated inflammation.