• 대한본초학회지
• /
• 제28권6호
• /
• pp.145-153
• /
• 2013

Objectives : Neuroinflammation is characterized by microglial activation and the expression of major inflammatory mediators. The present study investigated the inhibitory effect of ginsenoside Rg1 ($GRg_1$), a principle active ingredient in Panax ginseng, on pro-inflammatory cytokines and microglial activation induced by systemic lipopolysaccharide (LPS) treatment in the mouse brain tissue. Methods : Varying doses of $GRg_1$ was orally administered (10, 20, and 30 mg/kg) 1 h before the LPS injection (3 mg/kg, intraperitoneally). The mRNA expression of pro-inflammatory cytokines in the brain tissue was measured using the quantitative real-time PCR method at 4 h after the LPS injection, Microglial activation was evaluated using western blotting and immunohistochemistry against ionized calcium binding adaptor molecule 1 (Iba1) in the brain tissue. Cyclooxigenase-2 (COX-2) expressions also observed using western blotting and immunohistochemistry at 4 h after the LPS injection, In addition, double-immunofluorescent labeling of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and COX-2 with microglia and neurons was processed in the brain tissue. Results : $GRg_1$ (30 mg/kg) significantly attenuated the upregulation of TNF-${\alpha}$, interleukin (IL)-$1{\beta}$ and IL-6 mRNA in the brain tissue at 4 h after LPS injection. Morphological activation and Iba1 protein expression of microglia induced by systemic LPS injection were reduced by the $GRg_1$ (30 mg/kg) treatment. Upregulation of COX-2 protein expression in the brain tissue was also attenuated by the $GRg_1$ (30 mg/kg) treatment. Conclusion : The results suggest that $GRg_1$ is effective in the early stage of neuroinflammation which causes neurodegenerative diseases.

• 대한본초학회지
• /
• 제24권1호
• /
• pp.169-178
• /
• 2009

Objectives : In this study, the effects of ethylacetate extract of Ostericum koreanum on inflammation in RAW264.7 cells were investigated. Methods : Dried roots of Ostericum koreanum was extracted with 80% methanol for 24 h, and then fractionated with n-butanol, n-hexan and ethylacetate. RAW264.7 cells, a mouse macrophage line were incubated with different concentrations of the extract for 30 min and then stimulated with LPS at indicated times. Cell toxicity was determined by MTT assay. The concentrations of nitric oxide (NO) and prostaglandin E2 ($PGE_2$) were measured by Griess assay and enzyme immunoassay (EIA), respectively. The expressions of inducible nitric oxide synthease (iNOS) and cyclooxyganase (COX) -2 mRNA and protein were determined by RT-PCR and Western blot. Results : The methanol extract of Ostericum koreanuman and its fractions were significantly inhibited the NO and PGE2 productions in LPS-stimulated RAW264.7 cells. Among the fractions of Ostericum koreanuman the ethylacetate fraction was more strongly inhibited NO and $PGE_2$ productions compared with other fractions. The ethylacetate fraction was also suppressed LPS-induced mRNA expressions of iNOS and its protein levels in RAW264.7 cells. Conclusions : This study suggests that the ethylacetate fraction of Ostericum koreanum may have an anti-inflammatory property through suppressing inflammatory mediator productions in activated macrophages, suggesting have a therapeutic potential for the treatment of various inflammatory diseases.

• 한국식생활문화학회지
• /
• 제38권3호
• /
• pp.176-183
• /
• 2023

In this study, we investigated the effect of the extracts of Cyrtomium fortunei J.Sm. (CFJ) on lipopolysaccharide (LPS) induced inflammation in mouse BV-2 microglial cells. Nitric oxide (NO) production and cell viability were measured using the Griess reagent and the (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) (MTT) assay. Inflammatory cytokines were detected by quantitative polymerase chain reaction (qPCR) in BV-2 microglial cells with and without CFJ extracts. Subsequently, mitogen-activated protein kinases (MAPKs) and antioxidant markers were assessed by western blot analysis. It was found that the CFJ extract significantly decreased the production of pro-inflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-α, and IL-1β) and NO in BV-2 microglial cells that were stimulated with LPS. In addition, the expression levels of the phosphorylation of the MAPK family (p38, c-Jun N-terminal kinases [JNK], and extracellular-signal regulated kinase [ERK]) were reduced by CFJ. Also, treatment with CFJ significantly increased the activities of superoxide dismutase type 1(SOD1) and Catalase in BV-2 microglial cells. Our results indicate that CFJ has a potent suppressive effect on the pro-inflammatory responses of activated BV-2 microglia. Therefore, CFJ has the potential to be an effective treatment for neurodegenerative diseases, as it can inhibit the production of inflammatory mediators in activated BV-2 microglial cells.

• 한방재활의학과학회지
• /
• 제33권4호
• /
• pp.1-14
• /
• 2023

Objectives The anti-inflammatory and anti-arthritic effects of Youngseonjeatonguem (靈仙除痛飮, YSJTU) was evaluated in a cellular model using RAW264.7 macrophages, which are involved in osteoarthritis (OA), and an animal model using Sprague-Dawley (SD) rats, and a possible mechanism of anti-arthritic actions of YSJTU was presented. Methods RAW264.7 macrophages were activated by lipopolysaccharide (LPS). The production of pro-inflammatory cytokines (tumor necrosis factor [TNF]-𝛼, interleukin [IL]-1𝛽, and IL-6) and inflammatory mediators (nitric oxide [NO] and prostaglandin E2 [PGE2]) was determined by ELISA and Griess assay, respectively. Western blot was performed to determine inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. OA was induced by intra-articular injection of monosodium iodoacetate (MIA) into the right knee joint of SD rats. Results In RAW264.7 macrophages, YSJTU reduced LPS-induced production of TNF-𝛼, IL-1𝛽, and IL-6. In addition, YSJTU inhibited LPS-induced production of NO and PGE2 by suppressing iNOS and COX-2 expression. In SD rats, YSJTU improved MIA-induced OA by reducing swelling, skin heat, and cartilage degradation. In addition, YSJTU reduced serum levels of TNF-𝛼, IL-1𝛽, and IL-6, along with its significant decrease in serum levels of NO and PGE2. Conclusions These results suggest that YSJTU may exert anti-arthritic effect, at least in part, by inhibiting macrophage-mediated joint inflammation.

• 한국자원식물학회지
• /
• 제27권5호
• /
• pp.439-446
• /
• 2014

본 연구는 구실잣밤나무(C. cuspidate) 잎 추출물의 항염증 활성이 염증성 매개인자 생성 저해 및 염증성 사이토카인의 억제와 관련이 있을 것으로 예상되어짐에 따라, 구실잣밤나무를 대상으로 80% 에탄올를 가지고 추출한 후 추출물을 극성에 따라 순차적으로 용매분획을 실시하여, 구실잣밤나무 80% 에탄올 추출물 및 용매분획물들이 염증반응의 주체가 되는 대식세포 계열인 RAW 264.7 세포에서 LPS로 유도된 NO의 생성억제효과, 그리고 iNOS와 COX-2의 mRNA와 단백질 발현 억제효과 및 IL-6와 IL-$1{\beta}$와 같은 염증성 사이토카인 생성 억제효과 등을 알아보았다. 대식세포 계열인 RAW 264.7 세포에 LPS로 자극을 주고 구실잣밤나무 80% 에탄올 추출물 및 분획물을 처리하여 확인해본 결과, 헥산, 디클로로메탄 및 에틸아세테이트 분획물에서 NO의 생성억제 효과가 강하게 나타났으며, 헥산과 디클로로메탄 분획물에서는 iNOS와 COX-2 생성 억제 효과가 다른 분획물에 비해 강하게 나타났으며 염증성 사이토카인 생성 억제 효능도 80% 에탄올 추출물 및 분획물들이 다소 차이는 있었지만 헥산과 디클로로메탄 분획물에서 IL-6와 IL-$1{\beta}$에서 생성억제 효과가 나타났다. 이러한 결과는 구실잣밤나무 잎에서 유효성분 추출을 통한 항염증 물질의 연구 또는 예방하거나 치료할 수 있는 염증 억제 성분의 분리 및 그 작용기전 연구에 중요한 기초 자료가 될 것이라 사료된다. 또한 구실잣밤나무 추출물로부터 염증억제 성분을 도출하고자 활성분획인 디클로로 메탄 분획물에 대하여 활성성분의 분리가 진행 중이다.

• 대한본초학회지
• /
• 제22권3호
• /
• pp.117-125
• /
• 2007

Objective : Lonicera japonica (Caprifoliaceae) has long been used for treatment of infectious diseases in oriental countries. The aim of this study was to investigative the effect by which the aqueous extract from flower of L. japonica (LJFAE) inhibited the lipopolysaccharide (LPS)-induced inflammatory mediators in murine macrophages, RAW 264.7 cells Methods : The dried flowers of L. japonica were extracted with distilled water at $100^{\circ}C$ for 7 h. The extract was filtered through 0.45 ${\mu}m$ filter, freeze-dried. The dried extract was dissolved in Hank's balanced salt solution (HBSS) and filtered through 0.22 ${\mu}m$ filter before use. Accumulated nitrite, an oxidative product of nitric oxide (NO), was measured in the culture medium by the Griess reaction. The levels of prostaglandin E2 (PGE2), tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-1$\beta$ (IL-1$\beta$), and IL-6 production, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression were measured by enzyme-linked immunosorbent assay and Western blot analysis. Results: LJFAE (10-400 ${\mu}g$/ml) per se had no cytotoxic effect in unstimulated macrophages, but LJFAE concentration-dependently reduced NO, PGE2, TNF-, IL-l, and IL-6 production and COX-2 activity caused by stimulation of LPS. The levels of iNOS and COX-2 protein expressions were markedly suppressed by the treatment with LJFAE in a concentration dependent manner. Conclusions : These results suggest that LJFAE suppress the NO and PGE2production in macrophages by inhibiting iNOS and COX-2 expression and these properties may contribute to the anti-inflammatory activity of Lonicera japonica.

• Journal of Microbiology and Biotechnology
• /
• 제30권1호
• /
• pp.85-92
• /
• 2020

One of the omega-3 essential fatty acids, docosahexaenoic acid (DHA), is a significant constituent of the cell membrane and the precursor of several potent lipid mediators. These mediators are considered to be important in preventing or treating several diseases. Resolvin D5, an oxidized lipid mediator derived from DHA, has been known to exert anti-inflammatory effects. However, the detailed mechanism underlying these effects has not yet been elucidated in human monocytic THP-1 cells. In the present study, we investigated the effects of resolvin D5 on inflammation-related signaling pathways, including the extracellular signal-regulated kinase (ERK)-nuclear factor (NF)-κB signaling pathway. Resolvin D5 downregulated the production of interleukin (IL)-6 and chemokine (C-C motif) ligand 5 (CCL5). Additionally, these inhibitory effects were found to be modulated by mitogen-activated protein kinase (MAPK) and NF-κB in lipopolysaccharide (LPS)-treated THP-1 cells. Resolvin D5 inhibited the LPS-stimulated phosphorylation of ERK and translocation of p65 and p50 into the nucleus, resulting in the inhibition of IL-6 and CCL5 production. These results revealed that resolvin D5 exerts anti-inflammatory effects in LPS-treated THP-1 cells by regulating the phosphorylation of ERK and nuclear translocation of NF-κB.

• Journal of Ginseng Research
• /
• 제44권6호
• /
• pp.833-842
• /
• 2020

Background: Ulcerative colitis (UC) is a commonly encountered large intestine disease in the contemporary world that terminates into colorectal cancer; therefore, the timely treatment of UC is of major concern. Panax ginseng Meyer is an extensively consumed herbal commodity in South East Asian countries, especially Korea. It exhibits a wide range of biologically beneficial qualities for almost head-to-toe ailments in the body. Epimedium koreanum Nakai (EKN) is also a widely used traditional Korean herbal medicine used for treating infertility, rheumatism, and cardiovascular diseases. Materials and methods: Separately the anti-inflammatory activities of both red ginseng extracts (RGEs) and EKNs had been demonstrated in the past in various inflammatory models; however, we sought to unravel the anti-inflammatory activities of the combination of these two extracts in dextran sulfate sodium (DSS)-induced ulcerative colitis in mice model because the allopathic remedies for UC involve more side effects than benefits. Results: Our results have shown that the combination of RGE + EKN synergistically alleviated the macroscopic lesions in DSS-induced colitic mice such as colon shortening, hematochezia, and weight loss. Moreover, it restored the histopathological lesions in mice and decreased the levels of proinflammatory mediators and cytokines through the repression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP-3) expression. In vitro, this combination also reduced the magnitude of nitric acid (NO), proinflammatory mediators and cytokine through NF-κB and mitogen-activated protein kinase (MAPK) pathways in RAW 264.7 mouse macrophage cells. Conclusion: In the light of these findings, we can endorse this combination extract as a functional food for the prophylactic as well as therapeutic treatment of UC in humans together with allopathic remedies.

• 치위생과학회지
• /
• 제14권2호
• /
• pp.223-229
• /
• 2014

본 연구에서는 체내 염증지표 변화를 모니터링 함으로써 새로운 천연추출물인 polycan 및 calcium gluconate 복합제제의 치주질환 개선 효과를 평가하고자 하였으며, 다음과 같은 결론을 얻었다. 1. 치은열구액 내 $IL-1{\beta}$는 대조군과 시험군 모두 시간에 따른 유의한 차이는 없었으나(p>0.05), 4주째 시험군이 대조군보다 낮았다(p<0.05). 2. 치은열구액 내 MMP-8과 $TNF-{\alpha}$는 4주째 시험군에서 초기에 비해 감소하였으며, 시험군이 대조군보다 낮았다. 3. 혈액 내 MMP-8은 4주째 시험군에서 유의하게 감소하였고(p<0.05), 대조군에 비해 통계적으로 유의하게 낮았다(p<0.05). 그러나 혈액 내 CRP는 유의한 변화가 관찰되지 않았다(p>0.05). 이상의 결과들을 종합해 보았을 때, polycan을 함유한 calcium gluconate 복합제 복용이 전신적인 염증성 생체지표에 영향을 미쳐 치은열구액 내의 염증매개물질들을 감소시킴으로써 치은건강에 긍정적인 효과를 나타내는 것으로 사료된다.

• Journal of Ginseng Research
• /
• 제38권1호
• /
• pp.8-15
• /
• 2014

Helicobacter pylori-induced gastric inflammation includes induction of inflammatory mediators interleukin (IL)-8 and inducible nitric oxide synthase (iNOS), which are mediated by oxidant-sensitive transcription factor NF-${\kappa}B$. High levels of lipid peroxide (LPO) and increased activity of myeloperoxidase (MPO), a biomarker of neutrophil infiltration, are observed in H. pylori-infected gastric mucosa. Panax ginseng Meyer, a Korean herb medicine, is widely used in Asian countries for its biological activities including anti-inflammatory efficacy. The present study aims to investigate whether Korean Red Ginseng extract (RGE) inhibits H. pylori-induced gastric inflammation in Mongolian gerbils. One wk after intragastric inoculation with H. pylori, Mongolian gerbils were fed with either the control diet or the diet containing RGE (200 mg RGE/gerbil) for 6 wk. The following were determined in gastric mucosa: the number of viable H. pylori in stomach; MPO activity; LPO level; mRNA and protein levels of keratinocyte chemoattractant factor (KC, a rodent IL-8 homolog), IL-$1{\beta}$, and iNOS; protein level of phospho-$I{\kappa}B{\alpha}$(which reflects the activation of NF-${\kappa}B$); and histology. As a result, RGE suppressed H. pylori-induced mRNA and protein levels of KC, IL-$1{\beta}$, and iNOS in gastric mucosa. RGE also inhibited H. pylori-induced phosphorylation of $I{\kappa}B{\alpha}$ and increases in LPO level and MPO activity of gastric mucosa. RGE did not affect viable H. pylori colonization in the stomach, but improved the histological grade of infiltration of poly-morphonuclear neutrophils, intestinal metaplasia, and hyperplasia. In conclusion, RGE inhibits H. pyloriinduced gastric inflammation by suppressing induction of inflammatory mediators (KC, IL-$1{\beta}$, iNOS), MPO activity, and LPO level in H. pylori-infected gastric mucosa.