• Natural Product Sciences
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• 제14권3호
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• pp.206-213
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• 2008

This study was designed to investigate the anti-inflammatory effects of mangiferin isolated from the rhizome of Anemarrhena asphodeloides, a natural polyphenol, on lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Mangiferin dose-dependently inhibited LPS-induced nitric oxide (NO) and prostaglandin $E_2\;(PGE_2)$ productions in RAW 264.7 macrophages and peritoneal macrophages isolated from C57BL/6 mice. Consistent with these data, mangiferin suppressed the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels in a concentration-dependent manner, as determined by Western blotting and RT-PCR, respectively. In addition, the release of tumor necrosis $factor-{\alpha}$($TNF-{\alpha}$) and interleukin-6 (IL-6), and the mRNA expression levels of these cytokines were reduced by mangiferin in a dose-dependent manner. Moreover, mangiferin effectively inhibited the transcriptional activation of nuclear factor-kappa B $(NF-{\kappa}B)$. These results suggest that the anti-inflammatory properties of mangiferin are caused by iNOS, COX-2, $TNF-{\alpha}$, and IL-6 down-regulation due to $(NF-{\kappa}B)$ inhibition in RAW 264.7 macrophages.

• 생명과학회지
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• 제19권10호
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• pp.1396-1402
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• 2009

본 연구에서는 갈조류의 일종인 톳(H. fusiforme)의 항염증 효과에 관한 생화학적 기전 해석을 위하여 U937 단핵구 세포를 이용하였으며, PMA에 의하여 인위적으로 유발된 COX-2의 발현 및 $PGE_2$의 생성 증가에 미치는 몇 가지 톳 추출물의 영향을 조사하였다. PMA는 U937 세포에서 처리 농도 의존적으로 COX-2의 전사 및 번역수준의 발현을 증가시켰으나, COX-1의 발현에는 큰 변화가 없었다. PAM에 의한 COX-2의 발현 증가는 $PGE_2$ 생성 증가와 연관성이 있었고, 톳의 열수 추출물에 비하여 에탄올 및 메탄올 추출물은 COX-2의 발현 증가는 $PGE_2$ 생성 증가를 매우 억제시켰으나, COX-1의 발현에는 영향을 주지 않았다. 아울러 PMA에 의한 NF-$\kappa$B의 핵내 이동 및 I$\kappa$B의 분해를 톳의 에탄올 및 메탄올 추출물이 완벽하게 차단시켰다. 본 연구의 결과는 톳의 에탄올 및 메탄올 추출물이 NF-$\kappa$B의 활성을 차단함으로서 COX-2의 발현 및 $PGE_2$ 생성을 저해하였음을 의미하며, 이는 톳이 강력한 항염증 효능을 가지고 있음을 뒷받침하여 주는 것이다.

• International Journal of Oral Biology
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• 제42권4호
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• pp.149-153
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• 2017

Cyclooxygenase-2 (COX-2)-mediated prostaglandin $E_2$ ($PGE_2$) plays a key role in development and progression of inflammatory responses and Porphyromonas gingivalis is a common endodontic pathogen. In this study, we investigated induction of COX-2 and $PGE_2$ by P. gingivalis in human dental pulp cells (HDPCs). P. gingivalis increased expression of COX-2, but not that of COX-1. Increased levels of $PGE_2$ were released from P. gingivalis-infected HDPCs and this $PGE_2$ increase was blocked by celecoxib, a selective COX-2 inhibitor. P. gingivalis activated all three types of mitogen-activated protein kinases (MAPKs). P. gingivalis-induced activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) was demonstrated by the results of phosphorylation of $NF-{\kappa}B$ p65 and degradation of inhibitor of ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$). Pharmacological inhibition of each of the three types of MAPKs and $NF-{\kappa}B$ substantially attenuated P. gingivalis-induced $PGE_2$ production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce $PGE_2$.

• BMB Reports
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• 제48권8호
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• pp.467-472
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• 2015

Heat shock increases skin temperature during sun exposure and some evidence indicates that it may be involved in skin aging. The antioxidant response mediated by the transcription factor NF-E2-related factor 2 (Nrf2) is a critically important cellular defense mechanism that serves to limit skin aging. We investigated the effects of heat shock on collagenase expression when the antioxidant defense system was downregulated by knockdown of Nrf2. GSH and collagenases were analyzed, and the expression of inducible Nrf2, HO-1, and NQO1 was measured. HS68 cells were transfected with small interfering RNA against Nrf2. Heat shock induced the downregulation of Nrf2 in both the cytosol and nucleus and reduced the expression of HO-1, GSH, and NQO1. In addition, heat-exposed Nrf2-knockdown cells showed significantly increased levels of collagenase protein and decreased levels of procollagen. Our data suggest that Nrf2 plays an important role in protection against heat shock-induced collagen breakdown in skin. [BMB Reports 2015; 48(8): 467-472]

• 생물환경조절학회지
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• 제31권4호
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• pp.460-467
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• 2022

본 연구에서는 양액재배 시 발생되는 폐양액의 적절한 농업적 이용방안을 강구하기 위해 폐양액의 비료 효과시험, 토양컬럼 시험, 그리고 작물 재배시험을 수행하였다. 폐양액의 비료 효과시험은 무기질소를 기준으로 질소비료와 폐양액의 토양 처리에 따른 열무의 생육특성과 토양의 화학적 특성을 조사하였다. 폐양액 비료 효과시험과 작물 재배시험을 위한 토양에 대한 폐양액의 처리는 무처리; A, 질소비료 100%; B, 질소비료 70%+폐양액 30%; C, 질소비료 50%+폐양액 50%; D, 질소비료 30%+폐양액 70%; E 총 5개 처리구로 하였다. 토양컬럼 시험을 위한 토양에 대한 폐양액의 처리는 무처리, 질소비료 100%, 폐양액 50%+질소비료 50% 3개 처리구로 하였다. 폐양액의 화학성은 pH 6.0, EC 2.4dS·m^-1, 총인(T-P) 28mg·L^-1, 암모늄태 질소(NH₄-N) 5.0mg·L^-1, 질산태 질소(NO₃-N) 301mg·L^-1로 나타났다. 토양의 화학성은 pH 5.51, EC 0.31dS·m^-1, 유기물 2.08g·kg^-1, 질산태 질소 9.64mg·kg^-1, 암모늄태 질소 3.20mg·kg^-1으로 나타났다. 질소비료 50% 이하와 폐양액 50% 이상의 비율이 열무 생육에 효과가 높은 것으로 나타났다. 폐양액을 질소비료와 함께 혼합하여 적용한 C-E 처리구에서 토양의 이화학성은 질소비료만을 적용한 B 처리구와 통계적으로 유의한 차이가 없었다. 토양컬럼 시험 결과 질소비료 100%와 폐양액 50%+질산비료 50% 처리구의 NO₃와 NH₄의 농도는 큰차이가 없는 것으로 나타났다. 폐양액을 화학비료의 표준시비량을 기준으로 이용하여 토양에 처리하면 토양 내 질소 성분의 이동과 주변의 영향은 일반 화학비료와 유사하게 나타나는 것으로 판단된다. 열무 토경재배에 폐양액과 질소비료를 혼합하여 사용하면 폐양액의 재이용으로 환경적 부담도 줄일 수 있고, 질소비료의 사용량도 줄일 수 있어 농가에 경제적 부담 감소와 열무 생산량 증대 효과도 기대할 수 있다.

• 생명과학회지
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• 제20권3호
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• pp.388-395
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• 2010

본 연구에서는 콩 발효 산물 추출물의 항염증 효능에 관한 기초 자료를 제시하기 위하여 PMA에 의해 유도되는 COX-2의 발현 및 $PGE_2$의 생성 증가에 미치는 이들 추출물의 영향을 조사하였다. 본 연구에서 조사된 3가지 콩 발효 산물은 PMA에 의한 COX-2의 발현 증가를 매우 유의적으로 차단하였으며, 이는 $PGE_2$의 생성 억제와 연관성이 있었다. 아울러 PMA에 의한 NF-${\kappa}B$ 활성 증가 또한 콩 발효 산물들에 의하여 유의적으로 억제되었다. 이러한 결과들은 콩 발효 산물에 의한 NF-${\kappa}B$ 활성의 억제가 COX-2의 발현을 저하시켰으며, 이로 인한 $PGE_2$의 생성이 억제된 것으로 추정되어진다. 이러한 콩 발효 산물의 항염증 효과는 대두 추출물보다 아가콩 추출물에서 더욱 효과가 높게 나타났으며, 이는 향후 아가콩 추출물은 염증성 질환 예방/치료를 위한 적용 가능성이 매우 우수함을 제시하여 주는 결과이다.

• 대한한방소아과학회지
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• 제26권4호
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• pp.10-23
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• 2012

Objectives: Gagamyanggyeoksan (G-YGS) has been used to suppress allergic reaction, however, the cellular target of G-YGS and its mode of action remain unclear. The present study was designed to investigate the effect of extracted G-YGS on the PMA and lonomycin (PI)-induced activation of RBL-2H3. Methods: For this investigation, We examined IL-4, IL-13 mRNA expression by Real-Time PCR, IL-4, IL-13 production by ELISA analysis and manifestations of GATA-1, GATA-2, NF-AT1, NF-AT2, AP-1 and NF-${\kappa}B$ p65 transcription factors by western blotting, OVA-specific IgE, IL-4, IL-13 by mouse be sensitive to OVA. Results: Here we showed that treatment of RBL-2H3 mast cells with G-YGS, suppressed PI-induced production of Th2 cytokines including IL-4 and IL-13 in a dose dependent manner. The mRNA expression of IL-4 were completely abolished by G-YGS at the concentration of $100{\mu}g/ml$. Data from a stable cell lines consistently expressing IL-4. And the mRNA expression of IL-13 were abolished by G-YGS at the $200{\mu}g/ml$. But there is no difference between the $50{\mu}g/ml$, the $100{\mu}g/ml$ and the comparison. Results from the western blot analysis of transcription factors involving IL-4 and IL-13 expression indicated that it prominently decreased the expression of mast cell specific transcricption factors including GATA-1, GATA-2, NF-AT2, c-Jun, NF-${\kappa}B$ p65 but not c-Fos. And G-YGS suppressed IgE, IL-4, IL-13 in mouse be sensitive to OVA. Conclusions We suggested the anti-allergic activities of G-YGS might be mediated by down-regulation of Th2 cytokines such as IL-4 and IL-13 through the regulation of transcription factors as GATA-1, GATA-2, NF-AT2, c-Jun, NF-${\kappa}B$ p65.

• Journal of Periodontal and Implant Science
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• 제48권5호
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• pp.284-294
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• 2018

Purpose: Epithelial barrier dysfunction is involved in the pathophysiology of periodontitis and oral lichen planus. Estrogens have been shown to enhance the physical barrier function of intestinal and esophageal epithelia, and we aimed to investigate the effect of estradiol (E2) on the regulation of physical barrier and tight junction (TJ) proteins in human oral epithelial cell monolayers. Methods: HOK-16B cell monolayers cultured on transwells were treated with E2, an estrogen receptor (ER) antagonist (ICI 182,780), tumor necrosis factor alpha ($TNF{\alpha}$), or dexamethasone (Dexa), and the transepithelial electrical resistance (TER) was then measured. Cell proliferation was measured by the cell counting kit (CCK)-8 assay. The levels of TJ proteins and nuclear translocation of nuclear factor $(NF)-{\kappa}B$ were examined by confocal microscopy. Results: E2 treatment increased the TER and the levels of junctional adhesion molecule (JAM)-A and zonula occludens (ZO)-1 in a dose-dependent manner, without affecting cell proliferation during barrier formation. Treatment of the tight-junctioned cell monolayers with $TNF{\alpha}$ induced decreases in the TER and the levels of ZO-1 and nuclear translocation of $NF-{\kappa}B$. These $TNF{\alpha}-induced$ changes were inhibited by E2, and this effect was completely reversed by co-treatment with ICI 182,780. Furthermore, E2 and Dexa presented an additive effect on the epithelial barrier function. Conclusions: E2 reinforces the physical barrier of oral epithelial cells through the nuclear ER-dependent upregulation of TJ proteins. The protective effect of E2 on the $TNF{\alpha}-induced$ impairment of the epithelial barrier and its additive effect with Dexa suggest its potential use to treat oral inflammatory diseases involving epithelial barrier dysfunction.

• 대한본초학회지
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• 제32권2호
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• pp.107-114
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• 2017

Objectives : Tribulus terrestris $Linn{\acute{e}}$ (Tribuli Fructus; TF) has been used to treat hypochondrium, agalactia, nebula, itching and vitiligo in traditional Korean medicine. In this study, we investigated the effects of TF 30% ethanol extract on inflammatory responses in IgE-stimulated RBL-2H3 mast cells. Methods : TF extract was prepared by 30% ethanol. RBL-2H3 cells, a rat mast cell line, were treated with TF extract at different concentrations for 1 hr and then stimulated with DNP-IgE/HSA for indicated times. Cell viability was measured by WST-1 assay. The expression of inflammatory cytokines (IL-4, IL-13 and $IFN-{\gamma}$) mRNA was determined by reverse transcriptase-PCR, and the phosphorylation of ERK1/2, p38 and JNK MAP kinases (MAPKs) was determined by Western blot. The nuclear expression of $NF-{\kappa}B$ p65 in the cells was detected by Western blot and immunocytochemistry, respectively. Results : The treatment of TF extract at 0.1 and $0.2mg/m{\ell}$ significantly decreased the expression of IL-4 and IL-13 mRNA in IgE-stimulated RBL-2H3 mast cells, while significantly increased the expression of $IFN-{\gamma}$ mRNA. TF extract treatment was also inhibited the phosphorylation of ERK1/2, p38 and JNK MAPKs in IgE-stimulated RBL-2H3 mast cells in a dose-dependent manner. In addition, TF extract significantly blocked the translocation of $NF-{\kappa}B$ p65 into the nuclear of cells after IgE stimulation. Conclusions : These results indicate that TF extract inhibits inflammatory response in IgE-stimulated mast cells through blocking MAPKs/$NF-{\kappa}B$ pathway. This suggests that TF extract has an anti-inflammatory activity in mast cell activation.

• Biomolecules & Therapeutics
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• 제27권4호
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• pp.381-385
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• 2019

We attempted to examine anti-inflammatory and anti-oxidant effects of 4'-O-${\beta}$-D-glucosyl-5-O-methylvisamminol (GOMV), the first epigenetic inhibitor of histone phosphorylation at Ser10. While GOMV did not affect the viability of murine macrophage RAW 264.7 cells, it significantly suppressed lipopolysaccharide (LPS)-induced generation of prostaglandin $E_2$ ($PGE_2$) and nitric oxide (NO) through transcriptional inhibition of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). GOMV also scavenged free radicals in vitro, increased NF-E2-related factor 2 (NRF2), and activated antioxidant response element (ARE), thereby resulting in the induction of phase II cytoprotective enzymes in human keratinocyte HaCaT cells. Finally, GOMV significantly protected HaCaT cells against 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative intracellular damages. Together, our results illustrate that GOMV possesses anti-inflammatory and anti-oxidant activity.