• 한국식품영양학회지
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• 제27권3호
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• pp.400-405
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• 2014

최근 알로에 베라 섭취에 의한 독성 간염이 보고되고 있으나, 아직까지 알로에 베라의 간에 대한 염증 효과가 명확히 밝혀지지 않았다. 본 연구는 알로에 베라 에탄올 추출물이 간세포의 염증 발현에 미치는 영향과 그 기전을 밝히기 위해 수행되었다. $0.001{\sim}100{\mu}g/mL$의 알로에 베라 추출물을 HepG2 세포에 처리하여 MTT assay를 시행한 결과, 모든 농도에서 세포사멸이 유도되지 않았다. 그러나 모든 농도에서 알로에 베라 추출물은 염증성 사이토카인인 IL-8의 분비를 15.7~25.8%까지 유의적으로 증가시켰다(p<0.05). 또 다른 사이토카인인 M-CSF도 알로에 베라 추출물에 의해 36.3~61.5%까지 유의적으로 분비가 증가되었다(p<0.05). 본 연구 결과는 알로에 베라 추출물이 IL-8과 M-CSF와 같은 염증성 사이토카인 분비기전에 의해 간에 염증을 유발할 수 있음을 보여준다. 또한 알로에 추출물에 의해 유발될 수 있는 간염기전을 제시함으로써, 향후 수행될 추가 실험을 위한 기초 자료로 그 가치가 높을 것으로 사료된다.

• 한방재활의학과학회지
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• 제31권1호
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• pp.33-46
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• 2021

Objectives The aim of this study is to evaluate anti-inflammatory and anti-arthritic effects of Sogyunghwalhyel-tang-gamibang (SGHHTGB) in cell and animal models and also to suggest one of putative mechanisms underlying its anti-arthritic effects. Methods Enzyme-linked immunosorbent assay was applied to measure the concentrations of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and prostaglandin E2 (PGE2) in culture medium and blood serum and nitric oxide (NO) was assayed by Griess reagent. The expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were analyzed by Western blot method. Results In a cell model using RAW264.7 macrophages stimulated with the endotoxin lipopolysaccharide (LPS), the drug, at its non-cytotoxic concentrations, inhibited the production of the pro-inflammatory cytokine TNF-α, IL-1β and IL-6. In addition, it suppressed the expression of the inflammatory enzyme iNOS and COX-2, and reduced the synthesis of the enzyme product NO (as stable nitrite) and PGE2 in activated macrophages. Meanwhile, in an animal model using rheumatic arthritis (RA) mice induced with injection of type II collagen antibody (CAb) and LPS, the drug improved clinical symptom of arthritis and reduced paw thickness and inflammatory cell infiltration. In blood of RA mice, the drug reduced serum levels of TNF-α, IL-1β, IL-6, nitrite, and PGE2, all inflammatory mediators produced by activated macrophages. Conclusions SGHHTGB may ameliorate CAb and LPS-induced RA in mice, presumably by inactivating macrophages that are capable of initiating joint inflammation by producing pro-inflammatory cytokines and expressing inflammatory enzymes.

• 한국미생물·생명공학회지
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• 제48권3호
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• pp.310-315
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• 2020

본 연구는 와송에 유기용매를 활용하여 순차적으로 추출하여 항염증 활성에 대한 가능성을 평가하기 하기 위해 수행되었다. 대식세포에 와송 hexane 추출물을 전처리하고 LPS로 염증을 자극하여 염증과 관련한 세포내 신호전달 경로에 미치는 영향을 확인하고자 하였다. 대식세포에 와송 hexane 추출물은 LPS 자극에 의해 세포 독성이 나타나지 않았고, ROS의 생성을 억제하는 것으로 확인되었다. 또한, IL-1β, IL-2, IL-6, IP-10과 같은 전염증성 사이토카인의 분비를 mRNA 수준에서 확인한 결과 탁월하게 억제하였다. 이러한 전염증성 사이토카인의 생성 억제는 상위 전사인자인 AP-1과 IRF3의 조절을 통해 이루어지므로 이들을 단백질 수준에서 발현량을 확인하였다. 그 결과 c-Jun, c-Fos, IRF-3의 인산화 억제로 핵 내 전사활성이 제한되었을 것으로 생각된다. 이들 결과를 종합해볼 때, 와송 hexane 추출물은 염증 반응을 저해하는 효과가 있는 것으로 나타나 다양한 염증성 질환의 예방 및 개선에 유용하게 활용할 수 있을 것으로 생각된다.

• 동의생리병리학회지
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• 제19권5호
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• pp.1399-1404
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• 2005

In oriental medicine, Cheongpyehwadam-tang (CHT) has long been used for the cure of inflammatory diseases in the lung and bronchus such as bronchitis, bronchial asthma, pneumonia and tuberculosis. It's use is currently further extended for the treatment of allergic asthma. To investigate the anti-inflammatory effects of CHT, we investigated the effects of CHT on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and pro-inflammatory cytokines ($TNF-{\alpha}$, IL-6, and $IL-1{\beta}$) production, and on the level of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines expression in murine macrophage RAW 264.7 cells. CHT alone did not affect NO or pro-inflammatory cytokines production. In contrast, CHT inhibited LPS-induced NO and proinflammatory cytokines and the levels of LPS-induced iNOS and proinflarnmatory cytokine mRNA in a dose-dependent manner. CHT also inhibited the nuclear factor-kappa B (NF-kB) activation. Taken together, these results suggested that CHT inhibits the production of NO and pro-inflammatory cytokines in RAW 264.7 cells through blockade of NF-kB activation.

• 대한한의학방제학회지
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• 제18권1호
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• pp.169-179
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• 2010

The pistil of nelumbo nucifera (PNN) is used in the treatment of nocturnal pollution, hematemesis, epistaxis, metrorrhagia and diarrhoea in traditional medicine. The present study was examined to evaluate the effects of PNN on the production of pro-inflammatory mediators in vitro. After the treatment of PNN, cell viability was measured by MTT assay, nitric oxide (NO) production was monitored by measuring the nitrite content in culture medium. The protein bands were determined by immunoblot analysis and levels of cytokines were analyzed by sandwich immunoassays. In the MTT assay, the doses of PNN extract (0.03, 0.10 mg/ml) had no significant cytotoxicity. The increases of NO production and inducible nitric oxide synthase expression were detected in lipopolysaccharide(LPS)-activated Raw 264.7 cells compared with control, in contrast, these increases were significantly attenuated by pre-treatment with PNN. In cytokine assay, the massive pro-inflammatory cytokines such as tumour necrosis factor-$\alpha$, interleukin (IL)-$1{\beta}$ and IL-6 were induced in LPS-activated Raw 264.7 cells, but pre-treatment of Raw 264.7 cells with PNN caused inhibition (TNF-$\alpha$=14.17%, IL-$1{\beta}$=107.43%, IL-6=46.27%) the production of cytokines by LPS. In addition, PNN reduced prostaglandin E2 productions in a dose-dependent manner (0.03mg/ml=37.52%, 0.10 mg/ml=83.77%) as a consequence of the inhibition of cyclooxygenase-2 expression. Taken together, our data indicates that PNN can regulate the inflammatory response in macrophage cells activated by Gram-negative infection.

• 동의생리병리학회지
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• 제17권3호
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• pp.804-809
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• 2003

Kagam-bojungikgitang is the water extracts prepared from Ginseng Radix, Astragali Radix. Angelicae gigantis Radix, Astractylodis Rhizoma alba, Aurantii nobilis Pericarpium, Glycyrrhizae Radix, Artemisiae iwayomogii Herba, and Scutellariae Radix. This is a modified prescription of Bojungikgitang, which has been used for the treatment of indigestion, and immunological disease in oriental countries. In this study, the effects of Kagam-bojungikgitang and Bojungikgitang on the production of prostaglandin E₂ (PGE₂) and the expression of cyclooxygenase-2 (COX-2) were examined using RAW 264.7 macrophages activated with lipopolysaccharide (LPS). Both prescriptions dose-dependently reduced the release of PGE2 and expression of COX-2 caused by stimulation of LPS without cytotoxic effect. Kagam-bojungikgitang's inhibitory effects were better than Bojungikgitang in PGE2 production and COX-2 expression. Moreover, Kagam-bojungikgitang also attenuated markedly the production of tumor necrosis factor (TNF)-α, and IL-6 than Bojungikgitang in LPS-stimulated RAW 264.7 macrophages. These results suggest that Kagam-bojungikgitang decreases PGE2 and pro-inflammatory cytokine production in macrophages and these properties may contribute to the anti-inflammatory activity of Kagam-bojungikgitang.

• Biomolecules & Therapeutics
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• 제21권6호
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• pp.435-441
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• 2013

Emodin, a naturally occurring anthraquinone derivative isolated from Polygoni cuspidati radix, has several beneficial pharmacologic effects, which include anti-cancer, anti-diabetic, and anti-inflammatory activities. In this study, the authors examined the effect of emodin on the production of proinflammatory cytokines, such as, tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6, in mouse bone marrow-derived mast cells (BMMCs) stimulated with phorbol 12-myristate 13-acetate (PMA) plus the calcium ionophore A23187. To investigate the mechanism responsible for the regulation of pro-inflammatory cytokine production by emodin, the authors assessed its effects on the activations of transcriptional factor nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and mitogen-activated protein kinases (MAPKs). Emodin attenuated the nuclear translocation of (NF)-${\kappa}B$ p65 and its DNA-binding activity by reducing the phosphorylation and degradation of $I{\kappa}B{\alpha}$ and the phosphorylation of $I{\kappa}B$ kinase B (IKK). Furthermore, emodin dose-dependently attenuated the phosphorylations of MAPKs, such as, extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAP kinase, and the stress-activated protein kinases (SAPK)/c-Jun-N-terminal kinase (JNK). Taken together, the findings of this study suggest that the anti-inflammatory effects of emodin on PMA plus A23187-stimulated BMMCs are mediated via the inhibition of NF-${\kappa}B$ activation and of the MAPK pathway.

• Biomolecules & Therapeutics
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• 제20권5호
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• pp.457-462
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• 2012

The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin B in lipopolysaccharide (LPS)-stimulated peritoneal macrophage and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Of KP extracts, KP BuOH-soluble fraction most potently inhibited LPS-induced IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ expression, as well as NF-${\kappa}B$ activation. However, KP BuOH fraction increased IL-10, an anti-inflammatory cytokine. KP BuOH fraction also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. KP BuOH fraction also potently inhibited the expression of the pro-inflammatory cytokines, IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ as well as the activation of NF-${\kappa}B$. Kalopanaxsaponin B, a main constituent of KP, inhibited TNBS-induced colonic inflammation, including colon shortening, and TNBS-increased myeloperoxidase activity pro-inflammatory cytokine expression and NF-${\kappa}B$ activation in mice. Based on these findings, KP, particularly its main constituent, kalopanaxsaponin B, may ameliorate colitis by inhibiting NF-${\kappa}B$ pathway.

• 한국축산식품학회지
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• 제32권5호
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• pp.635-643
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• 2012

As an appraisal for the application of a new starter culture, more than 200 lactic acid bacteria strains were isolated from raw milk and healthy human feces. The strains showing excellent growth and acid production ability in 10% skim milk media were selected and identified as Lactobacillus casei based on the results of their API carbohydrate fermentation patterns, as well as 16S rDNA sequence analysis. To assess the effect of L. casei strains on irritable bowel disease (IBD), the inhibitory effect of the selected strains against the nitric oxide (NO) production of lipopolysaccharide (LPS)-stimulated RAW 264.7 cells was measured. Among the tested L. casei strains, L. casei MCL was observed to have the greatest NO inhibitory activity. Additionally, L. casei MCL was found to inhibit mRNA expression of pro-inflammatory cytokines (interleukin-$1{\beta}$, IL-6, TNF-${\alpha}$), as well as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) involved in pathophysiologic processes such as inflammation. The mRNA expression of anti-inflammatory cytokines, including IL-10 and transforming growth factor-$1{\beta}$ (TGF-${\beta}$) of L. casei MCL, was confirmed using quantitative real-time PCR. In conclusion, L. casei MCL showed decreases in the expression of pro-inflammatory cytokines and up-regulated expression of the anti-inflammatory cytokine.

• BMB Reports
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• 제46권7호
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• pp.376-381
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• 2013

It is unknown how soluble pattern-recognition receptors in blood, such as mannose-binding lectin (MBL) and ficolins, modulate mast cell-mediated inflammatory responses. We investigate how mouse MBL-A or ficolin-A regulate mouse bone marrow-derived mast cells (mBMMCs)-derived inflammatory response against bacterial lipopolysaccharide (LPS) stimulation. LPS-mediated pro-inflammatory cytokine productions on mBMMCs obtained from Toll-like receptor4 (TLR4)-deficient mice, TLR2-defficient mice, and their wildtype, were specifically attenuated by the addition of either mouse MBL-A or ficolin-A in a dose-dependent manner. However, the inhibitory effects by mouse MBL-A or ficolin-A were restored by the addition of mannose or N-acetylglucosamine, respectively. These results suggest that mouse MBL-A and ficolin-A bind to LPS via its carbohydrate-recognition domain and fibrinogen-like domain, respectively, whereby cytokine production by LPS-mediated TLR4 in mBMMCs appears to be down-regulated, indicating that mouse MBL and ficolin may have an inhibitory function toward mouse TLR4-mediated excessive inflammation on the mast cells.