• Korean Journal of Plant Resources
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• v.31 no.4
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• pp.294-302
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• 2018

This study was conducted to compare anti-inflammatory effect of Robinia pseudoacacia L. using different extraction methods (water extraction, ethanol extraction and high temperature extraction). We investigated anti-inflammatory effect of Robinia pseudoacacia L. extract (RP1, water extract; RP2, ethanol extract; RP3, high temperature extract) on lipopolysaccharide (LPS)-stimulated inflammation using Raw 264.7 cell. Cells were treated with various concentrations (12.5, 25, 50, 100 or $200{\mu}g/m{\ell}$) of water extract, ethanol extract and high temperature extract. Cytotoxicity was not observed on Raw 264.7 cells, LPS-stimulated production of NO (nitric oxide), $PGE_2$ (prostaglandin $E_2$) and cytokines ($TNF-{\alpha}$, IL-6 and $IL-1{\beta}$) was reduced by RP3 treatment more than RP1 and RP2. In conclusion, these results indicated that inflammation on Raw 264.7 cells was improved by RP3. Treatment of RP3 could be used to natural medicine for improving inflammatory response. However, further experiment is required to observe how the high temperature extraction at $500^{\circ}C$ for 48 h influences on alteration of active ingredient in Robinia pseudoacacia L., and conducts the inflammation signal pathway on Raw 264.7 cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.6
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• pp.681-687
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• 2017

This study was focused on the anti-inflammatory activities of Annona muricata leaf ethanol extracts (AME). Inflammation of macrophages was induced by lipopolysaccharide (LPS) treatment, and various inflammation-mediated factors [cytokines and nitric oxide (NO)] were measured. AME treatment significantly reduced LPS-induced NO, cytokine levels [interleukin (IL)-6, tumor necrosis $factor-{\alpha}$ and $IL-1{\beta}$], and expression of inducible NO synthase and cyclooxygenase-2 in a dose-dependent manner. Mechanical studies showed that AME treatment inhibited activation of mitogen-activated protein kinase and nuclear factor $(NF)-{\kappa}B$ in macrophages treated with LPS. From these results, AME treatment strongly inhibits LPS-induced inflammation through inhibition of $NF-{\kappa}B$ activation, suggesting AME could be a potential candidate for treatment of inflammatory disease as a nutraceutical drug.

• Korean Journal of Microbiology
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• v.55 no.3
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• pp.213-219
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• 2019

Acne is a chronic inflammatory disease outbreak in the sebaceous glands within the hair follicle. The proliferation of Propionibacterium acnes (P. acnes) causes monocytes to stimulate secretion of inflammatory cytokines. A number of studies proposed the inhibitory effects of P. acnes-mediated inflammation by several natural extracts. However, studies on the effect of Eurya persicifolia Gagnep. (E. persicifolia) extracts on the inflammatory responses by P. acnes have not been explored yet. In this study, we investigated the anti-inflammatory effect of E. persicifolia extract in the inflammatory reactions induced by P. acnes. We found that E. persicifolia extract successfully diminished the expression levels of inflammatory mediators such as IL-$1{\beta}$, IL-6, TNF-${\alpha}$, and iNOS in P. acnes-activated mouse macrophage RAW 264.7 cells. We found that the immunosuppressive effect of E. persicifolia extract in the P. acnes-activated inflammatory signaling is mediated by the regulation of NF-${\kappa}B$ transcriptional activation, which is a key regulator of inflammatory cytokine expression. Our results suggest that E. persicifolia extract held potentials for the treatment of P. acnes by suppressing NF-${\kappa}B$ signaling pathways.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.41 no.1
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• pp.45-55
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• 2015

Ultraviolet B (UVB) irradiation induces both production of reactive oxygen species (ROS) and glucocorticoids (GCs)-mediated stress responses such as an increase of $11{\beta}$-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1) activity in skin. In addition, ROS-induced inflammatory mediators and proinflammatory cytokines trigger skin inflammation. In this study, as $11{\beta}$-HSD1 inhibitor recovered a decrease of catalase expression, we investigated whether Trapa japonica (TJ) extract and its fractions could inhibit $11{\beta}$-HSD1/ROS-induced skin inflammation in HaCaT keratinocytes. TJ extract and its fractions inhibited expressions of $11{\beta}$-HSD1 as well as the increase of ROS in UVB-exposed HaCaT keratinocytes. Moreover, proinflammatory cytokines such as interleukin (IL)- ${\alpha}$, - ${\beta}$ and tumor necrosis factor (TNF)-${\alpha}$, and cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) as inflammatory mediators were also inhibited in both mRNA and protein levels. Finally, prostaglandin $E_2$ ($PGE_2$) produced by COX-2 was inhibited effectively by TJ extract and its fractions. Taken together, these results suggest that TJ extract could be a potential anti-inflammatory ingredient to inhibit UVB-induced inflammation in skin.

• Journal of the Korea Convergence Society
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• v.12 no.2
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• pp.295-300
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• 2021

This study was conducted to investigate the effect of Celeriac Extract on the production of pro-inflammatory cytokines. Inflammation is caused by pro-inflammatory cytokines TNF-α, IL-6, IL-1β and mediators such as free radicals. We investigated the effect of Celeriac Extract (1ug/mL, 10ug/mL, 100ug/mL) on the production of proinflammatory cytokines such as TNF-α, IL-6, IL-1β and NO by lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. These results demonstrated that Celeriac Extract inhibited the production of TNF-α, IL-6 and NO, without cytotoxicity significantly. Therefore, these findings suggest that Celeriac Extract may attenuate inflammatory responses via inhibition of production of pro-inflammatory cytokines and NO.

• Journal of Applied Biological Chemistry
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• v.64 no.4
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• pp.375-382
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• 2021

Biorenovation is a microbial enzyme-based structural modification of component compounds in natural products and synthetic compounds including plant extracts with the potential benefits of improved biological activities compared with its reaction substrates. In this study, we investigated the anti-inflammatory activity of Distylium racemosum leaf extract and D. racemosum leaf biorenovation extract (DLB). As a result, DLB inhibited nitric oxide, prostaglandin E2, and inflammatory cytokines including tumor necrosis factor-α, interleukin-6, interleukin-1β at non-toxic concentrations. In addition, DLB significantly inhibited inducible nitric oxide synthase and cyclooxygenase-2 on LPS-treated RAW 264.7 macrophages. Based on these results, we suggest that the DLB could be used as a potent anti-inflammatory agents. It also suggests that the application of biological evolution has potential usefulness to increase the practical value of natural products.

• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.37 no.1
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• pp.67-73
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• 2011

Dental bacteria can cause gum diseases, i.e. gingivitis and periodontitis, by inducing inflammation in human gingiva. Therefore, the most effective way to prevent and treat gum diseases is the control of the inflammatory reactions induced by dental bacteria. Almost all present dental care products contain anti-bacterial agents to eliminate dental bacteria. However, recent studies report that even heat-killed dental bacteria can induce the inflammation responses in oral cells. Therefore, the method using anti-bacterial agents should be improved for better anti-inflammatory effect and the effective natural anti-inflammatory substances need to be found. In addition, the mechanisms of gingival inflammation should be elucidated. In this study, we tried to find out the mechanism of the gingival inflammation and effective natural anti-inflammatory substances with human gingival epithelial cells and Prevotella intermedia which is well known as a typical dental bacteria inducing gingivitis and periodontitis. In results, Prevotell intermedia initiated the gingival inflammation response by stimulating gingival epithelial cells to release an inflammatory cytokine, IL-8. Furthermore, the inflammation by Prevotella intermedia is related to COX-2, AP-1, and TNF-${\alpha}$ pathways. Green tea extract could effectively suppress the inflammatory responses induced by Prevotella intermedia. We find out the effective natural substance for the improvement of gum diseases by studying the mechanism of the gingival inflammation induced by dental bacteria.

• Journal of Acupuncture Research
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• v.25 no.2
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• pp.75-89
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• 2008

목적 : 후박(厚朴)(Magnolia obovata)에서 추출한 낮은 농도의 obovatol 약침액의 RAW264.7 세포에서 LPS로 유발된 염증, $TNF-{\alpha}$로 유발된 human colon carcinoma SW620 및 HCT116 세포의 세포증식에 대한 영향과 그 기전을 살펴보고자 하였다. 방법 : RAW264.7 세포에서 LPS로 염증을 유발하고 낮은 농도의 obovatol 약침액을 처리한 후 cell viability, NO 생성량, iNOS와 COX-2의 발현, $NF-{\kappa}B$활성, 전사능력을 관찰하기 위해 WST-1 assay, NO determination assay, western blot analysis, EMSA, luciferase activity assay를 시행하였고, HCT116, SW620 세포에 $TNF-{\alpha}$로 증식을 유도하고 낮은 농도의 obovatol 약침액을 처리한 후 cell growth, apoptosis 및 apoptosis와 연관된 $NF-{\kappa}B$의 활성 변화를 관찰하기 위해 WST-1, Cell morphogy test, DAPI staining and TUNEL assay, EMSA, luciferase activity assay를 시행하였다. 결과 : 1. RAW264.7 세포에서 낮은 농도의 obovatol 약침액 처리는 $NF-{\kappa}B$의 활성 및 전사능력을 낮추고 iNOS와 COX-2의 발현과 NO 생성을 감소시켜 LPS로 유발된 염증을 억제하였다. 2. HCT116, SW620 세포에서 낮은 농도의 obovatol 약침액 처리는 $NF-{\kappa}B$의 활성을 낮추어 세포자멸사를 촉진함으로써 $TNF-{\alpha}$로 유발된 암세포의 성장을 억제하였다. 결론 : 이상의 결과는 낮은 농도의 obovatol 약침액이 항염 및 인간 전립선암세포주인 SW620, HCT116에 대한 증식억제 효과가 있음을 입증한 것이며, 향후 이를 바탕으로 한 생체 연구에서의 긍정적인 결과는 obovatol 약침액이 만성염증성 질환 및 대장암의 예방과 치료에 대한 효과적인 치료제 개발에 초석이 될 것으로 기대된다.

• Korean Journal of Microbiology
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• v.50 no.3
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• pp.261-263
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• 2014

Chronic inflammation is involved in cancers, rheumatoid arthritis, and Crohn's disease. Inerleukin-6 (IL-6) plays major roles in inflammation. Chungkookjang, fermented soybean contains diverse peptides produced by cleavage of soybean proteins. The peptides can be bioactive compounds. Peptide (Gly-Val-Tyr-Tyr-Met-Tyr was purified from Chungkookjang, and modified to be 6mer H, Glu-Val-Tyr-Tyr-Met-Tyr (EVYYMY). Peptide H's activity to suppress IL-6 expression in a human breast cancer cell, MDA-MB-231 was determined. IL-6 Expression was reduced in the cell treated with peptide H 25 times less than controls which were not treated with peptide H. Proliferation of MDA-MB-231 cells was inhibited by peptide H, which is concentration-dependent. Blocking of IL-6 signals is known to be effective in reducing inflammation in rheumatoid arthritis, Crohn's disease, and cancers. Since peptide H can reduce inflammatory IL-6 expression, application of this study will contribute to drug development for diseases which are caused by excessive IL-6.