• Proceedings of the Plant Resources Society of Korea Conference
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• 2020.12a
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• pp.73-73
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• 2020

Toona sinensis (TS) leaf is known to antinociceptive, antioxidative stress and skin moisturizing effects. Acnes vulgaris is a chronic skin disease with various symptoms including itchiness, pain and interruption of normal skin function. Propionibacterium acnes (P. acnes) is a major factor in the occurrence of inflammatory acnes. This study evaluated the antioxidant and anti-inflammation effects by TS extract from adventitious shoots. TS extract showed anti-inflammatory activities by suppression of pro-inflammation mediators (iNOS and COX-2) in LPS-stimulated RAW264.7 cells. TS extract also has anti-inflammatory activities by inhibiting the secretion of pro-inflammatory cytokines on P. acnes-stimulated HaCaT cells. These effects were regulated by MAPK signaling pathway. Therefore, we suggest that TS extract from adventitious shoots might have applications as a medicine for treating P. acnes-induced skin diseases.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2018.10a
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• pp.128-128
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• 2018

Nypa fruticans wurmb (NF) has been used as traditional medicinal food in Asian countries. Especially, NF has been used for conventional medicine to treat inflammatory periodontal diseases. Previous studies have been shown that NF has large amount of useful constituents such as phenolic acids, polyphenols and flavonoids. Also, NF is known as having medicinal effects such as anti-oxidant, anti-inflammatory and cholesterol-lowering effects. NF has recently been attracted to use complementary medicinal food on inflammatory diseases in Korea. However, there are no obvious effects in inflammatory and metabolic diseases also mechanisms has been studied yet. The purpose of this study was to investigate the anti-inflammatory effects of NF and steamed-NF (SNF), which recently has been used as health food, using Human keratinocyte cell line (HaCaT) and Human mast cell line (HMC-1). The cytotoxicities of NF and SNF were measured by using MTT assays in HaCaT cells and HMC-1 cell. To evaluate anti-inflammatory effects of NF and SNF, HaCaT cells were stimulated with tumor necrosis factor $(TNF)-{\alpha}$ and Interferon $(IFN)-{\gamma}$. Also, HMC-1 cells were stimulated with phorbol-12-myristate-13-acetate (PMA) and A23187 calcium ionophore (A23187) to induce allergic inflammation. Inflammatory cytokine were measured by enzyme-linked immunosorbent assay (ELISA). In this result, the extract of NF and SNF (0.01 - 1mg/ml) did not show cytotoxicity in HaCaT cells and HMC-1 cells. In addition, the NF and SNF suppressed the production of interleukin (IL)-6 and IL-8 in HaCaT cells at highest concentration. Furthermore, the treatment of SNF significantly inhibited the secretion level of IL-8 in PMA plus A23187-stimulated HMC-1 cells compared with NF treatment group. These results suggest that the extract of NF and SNF may serve as a potential therapy for skin inflammatory diseases.

• Journal of Periodontal and Implant Science
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• v.38 no.3
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• pp.511-520
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• 2008

Purpose: Diabetes mellitus is a clinically and genetically heterogeneous group of metabolic disorders manifested by abnormally high levels of glucose in the blood. Mounting evidence demonstrates that diabetes is a risk factor for gingivitis and periodontitis. The circulating mononuclear phagocytes in diabetic patients with hyperglycemia are chronically exposed to high level of serum glucose. Thus, this study attempted to determine the effect of pre-exposure of monocytes and macrophages to high concentration of glucose on lipopolysaccharide (LPS)-induced production of pro-inflammatory mediators. Material and Methods: For this purpose, cells were cultured in medium containing normal (5 mM) or high glucose (25 mM) for 4-5 weeks before treatment for 24 h with LPS. LPS was highly purified from Porphyromonas gingivalis or Prevotella intermedia by phenol extraction. Result: Results showed that prolonged pre-exposure of cells to high glucose markedly increased LPS-stimulated NO secretion when compared to normal glucose. In addition to NO, high glucose also augmented LPS-stimulated IL-6, IL-8, and TNF-$\alpha$ secretion after cells were exposed to high glucose for 4 weeks. Conclusion: The present study demonstrates that pre-exposure of mononuclear phagocytes with high glucose augments LPS-stimulated production of pro-inflammatory mediators. These findings may explain why periodontal tissue destruction in diabetic patients is more severe than that in non-diabetic individuals.

• Korean Journal of Pharmacognosy
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• v.50 no.2
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• pp.102-111
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• 2019

Inflammation that is considered to be mainly related to pathogenesis of atopic dermatitis (AD) is the biological response of a host to stimuli, such as cellular injury or infection. In this study, we investigated the anti-inflammatory and anti-oxidative activities of white ginseng roots by ultra high pressure extraction (Gin-UHP), fermentation followed by ultra high pressure extraction (Gin-UHPF), and polyol extraction (Gin-POL). As a result, ginseng extracts were able to decrease the secretion of pro-inflammatory cytokines (interleukin-8 and tumor necrosis factor-alpha) and immunoglobulin E. Also, Gin-POL had the highest DPPH radical scavenging activity and when we compared the SOD-like activity, Gin-UHP had the highest. Moreover, we looked into the effect of these ginseng extracts on anti-aging to show the possible usefulness as a raw material of cosmetics. As a result, ginseng extracts were able to reduce the production of melanin, and inhibit the tyrosinase and elastase activities in a dose-dependent manner. The extracts also decreased the expression of MMP-1 and had a significant hyaluronidase inhibitory activity. Taken together, these results demonstrate that ginseng extracts may have an improvement effect on AD by using its anti-inflammatory and antioxidant properties.

• YAKHAK HOEJI
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• v.53 no.6
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• pp.321-327
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• 2009

Licochalcone A is a chalcone isolated from the roots of Glycyrrhiza inflate. In this study, we examined the effects of licochalonce A on the production of cytokines in LPS-activated macrophages. Licochalcone A inhibited the secretion of proinflammatory cytokines such as IL-1$\beta$, IL-6, and TNF-$\alpha$. The reduced secretion of proinflammatory cytokines is related to the differences in the mRNA expression of IL-1$\beta$, IL-6, and TNF-$\alpha$. Moreover, licochalcone A inhibited the mRNA expression of IL-12p40, IL-18, and IL-23p19. To investigate its mechanism, we performed gel shift assay. Licochalcone A reduced nuclear NF-${\kappa}B$ binding activity in LPS-activated RAW264.7 cells. Taken together, these results suggest that licochalcone A has anti-inflammatory effects in LPS-activated macrophages and its mechanism could be through the down-regulation of binding to the ${\kappa}B$ site.

• The Korea Journal of Herbology
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• v.30 no.5
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• pp.45-49
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• 2015

Objectives : The aim of this study is to investigate anti-inflammatory activity using various extracts of rice straw (DaoCao) extract (RS).Methods : To investigate the anti-inflammatory effect of RS, we examined the effect of RS on cytokines production on THP-1 cell. Cells were cultured in incubator (37℃, CO₂5%, 0.5% FBS-RPMI, 1X10⁶cells/ml). One hour after,Dermatophagoides pteronissinus(Dp., 10 ug/ml) was treated into cell and at 6 hour after, each different concentrations(0.1, 1 and 10 ug/ml) of RS were treated. The cells were incubated for 16 hours and harvest the supernatant. The levels of IL-4, IL-5, IL-6, IL-8, MCP-1 and TNF-αwere determined using a commercially available ELISA kit.Results : We investigated whether RS has the inhibition of inflammatory response in Jurkat cells and THP-1 cells. RS suppressed secretion of IL-4, IL-5, and TNF-αinduced by house dust mites in Jurkat cells. It showed significant effects for all concentrations. RS suppressed the increased expression of IL-6, IL-8 and MCP-1 after treatment with mite in THP-1 cells. These results suggest that RS may be used as a valuable agent for treating allergic diseases such as atopy due to its anti-inflammatory property.Conclusions : RS showed significant biological activities with anti-inflammatory in the human T cells. These results suggest that RS may be used as a valuable agent for treating allergic diseases such as atopy due to its anti-inflammatory property. In terms of Korean traditional medicine, we expect the results to contribute to building of EBM (Evidence-Based Medicine).

• Nutrition Research and Practice
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• v.11 no.5
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• pp.357-364
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• 2017

BACKGROUND/OBJECTIVES: Oxidative stress is closely related with inflammation and development of many diseases. Black soybean seed coat contains high amount of anthocyanins, which are well-known for free radical scavenging activities. This study investigated inflammatory response and action mechanism of black soybean anthocyanins with regard to antioxidant activity in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. MATERIALS/METHODS: RAW 264.7 cells were treated with anthocyanins extracted from black soybean seed coats in a concentration range of 12.5 to $100{\mu}g/mL$. The production of reactive oxygen species (ROS), secretion of pro-inflammatory mediators and cytokines, and the signaling in the mitogen activated protein kinases (MAPKs) pathway were examined. RESULTS: Black soybean anthocyanins significantly decreased LPS-stimulated production of ROS, inflammatory mediators such as nitric oxide (NO) and prostaglandin $E_2$, and pro-inflammatory cytokines, including tumor necrosis factor ${\alpha}$ and interleukin-6, in a dose-dependent manner without cytotoxicity (P < 0.001). Black soybean anthocyanins downregulated the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated RAW 264.7 cells (P < 0.001). Moreover, black soybean anthocyanins inhibited LPS-induced phosphorylation of MAPKs, including extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 (P < 0.001). CONCLUSION: These results suggest that black soybean anthocyanins exert anti-inflammatory activity by inhibiting ROS generation and subsequent MAPKs signaling, thereby inhibiting inflammatory responses.

• Journal of Applied Biological Chemistry
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• v.62 no.3
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• pp.239-246
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• 2019

In this study, an evaluation of the anti-inflammatory effect of ferulic acid isolated from Tetragonia tetragonioides in lipopolysaccharide (LPS) simulated RAW 264.7 cells was made. The chemical structure of the active compound was elucidated by $^1H$-NMR, $^{13}C$-NMR, and FAB-MS, and was confirmed to be ferulic acid. Ferulic acid was purified via open column chromatography with Sephadex LH-20 and MCI gel CHP-20. To test the anti-inflammatory effect of ferulic acid, LPS-stimulated RAW 264.7 cells were treated in subsequent experiments with different concentrations of ferulic acid (5, 10, and $25{\mu}g/mL$) and the levels of inflammatory cytokines and enzymes were also measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay. Cell viability was above 95% at acid concentrations ranging from $5-25{\mu}g/mL$. The results showed that 30% of the production of nitric oxide and 66% of prostaglandin $E_2$ were inhibited by $25{\mu}g/mL$ of ferulic acid, it also inhibited the protein expression of both inducible nitric oxide synthase and cyclooxygenase-2 by 70%. Additionally, it inhibited the production of the pro-inflammatory cytokines, tumor necrosis factor-${\alpha}$, interleukin-6, and interleukin-$1{\beta}$ by 40, 75, and 77%, respectively. According to these results, the anti-inflammatory activity of ferulic acid was demonstrated via his implication in the inhibition of the expression and secretion of inflammatory substances in LPS-stimulated RAW 264.7 cells. Therefore, we concluded that ferulic acid can be used as a functional additive having anti-inflammatory activity.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.685-696
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• 2021

In this study, we investigated the inhibitory effect of 5-aminolevulinic acid (ALA), a heme precursor, on inflammatory and oxidative stress activated by lipopolysaccharide (LPS) in RAW 264.7 macrophages by estimating nitric oxide (NO), prostaglandin E2 (PGE2), cytokines, and reactive oxygen species (ROS). We also evaluated the molecular mechanisms through analysis of the expression of their regulatory genes, and further evaluated the anti-inflammatory and antioxidant efficacy of ALA against LPS in the zebrafish model. Our results indicated that ALA treatment significantly attenuated the LPS-induced release of pro-inflammatory mediators including NO and PGE2, which was associated with decreased inducible NO synthase and cyclooxygenase-2 expression. ALA also inhibited the LPS-induced expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, reducing their extracellular secretion. Additionally, ALA abolished ROS generation, improved the mitochondrial mass, and enhanced the expression of heme oxygenase-1 (HO-1) and the activation of nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) in LPS-stimulated RAW 264.7 macrophages. However, zinc protoporphyrin, a specific inhibitor of HO-1, reversed the ALA-mediated inhibition of pro-inflammatory cytokines production and activation of mitochondrial function in LPS-treated RAW 264.7 macrophages. Furthermore, ALA significantly abolished the expression of LPS-induced pro-inflammatory mediators and cytokines, and showed strong protective effects against NO and ROS production in zebrafish larvae. In conclusion, our findings suggest that ALA exerts LPS-induced anti-inflammatory and antioxidant effects by upregulating the Nrf2/HO-1 signaling pathway, and that ALA can be a potential functional agent to prevent inflammatory and oxidative damage.

• BMB Reports
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• v.51 no.10
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• pp.538-543
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• 2018

Pancreatic beta cell destruction and dysfunction induced by cytokines is a major cause of type 1 diabetes. Paraoxonase 1 (PON1), an arylesterase with antioxidant activity, has been shown to play an important role in preventing the development of diabetes in transgenic mice. However, no studies have examined the anti-diabetic effect of PON1 delivered to beta cells using protein transduction. In this study, we expressed the cell-permeable PON1 fused with PEP-1 protein transduction domain (PEP-1-PON1) to investigate whether transduced PEP-1-PON1 protects beta cells against cytokine-induced cytotoxicity. PEP-1-PON1 was effectively delivered to INS-1 cells and prevented cytokine-induced cell destruction in a dose-dependent manner. Transduced PEP-1-PON1 significantly reduced the levels of reactive oxygen species (ROS) and nitric oxide (NO), DNA fragmentation, and expression of inflammatory mediators, endoplasmic reticulum (ER) stress proteins, and apoptosis-related proteins in cytokine-treated cells. Moreover, transduced PEP-1-PON1 restored the decrease in basal and glucose-stimulated insulin secretion induced by cytokines. These data indicate that PEP-1-PON1 protects beta cells from cytokine-induced cytotoxicity by alleviating oxidative/nitrosative stress, ER stress, and inflammation. Thus, PEP-1-mediated PON1 transduction might be an effective method to reduce the extent of destruction and dysfunction of pancreatic beta cells in autoimmune diabetes.