• Korean Journal of Pharmacognosy
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• v.45 no.3
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• pp.256-261
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• 2014

Bee venom (BV) therapy has been used as a traditional medicine to treat a variety of conditions, such as arthritis, back pain, cancerous tumors, and skin diseases. However, regulatory effects of BV on tumor necrosis factor (TNF)-${\alpha}$-induced HaCaT cell migration or anti-inflammatory have not been explored. In the present study, we investigated the effects of BV on HaCaT cell migration and anti-inflammation. HaCaT cell migration was evaluated by wound-healing assay. The pro-inflammatory cytokines such as TNF-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-8 were examined by ELISA or Western blotting. BV treatment led to an increase in migration of HaCaT cells for 24 and 48 h. Especially, 10 ng/ml of BV were significantly increased HaCaT cell migration. Also, BV suppressed the secretion of TNF-${\alpha}$, IL-$1{\beta}$, and IL-8 in culture medium with HaCaT cells. In addition, Western blot results demonstrate that BV suppressed the expression of TNF-${\alpha}$ and IL-$1{\beta}$, in HaCaT cells. Especially, 1 or 10 ng/ml of BV markedly decreased the expression of pro-inflammatory cytokines. These results demonstrate the potential of BV for the prevention of skin inflammation induced by TNF-${\alpha}$.

• Journal of Life Science
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• v.10 no.4
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• pp.362-364
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• 2000

Opuntia ficus-indca(Op) extract has been claimed to have several therapeutic properties in oriental medicine including anti-inflammatory and anti-rheumatoid arthritis effects. Little is known of its effect on the activation of immune cells such as T cells and macrophages. To evaluate the functional effect of Op extract on immune cells, we examined whether Op extract stimulates the proliferation of T cells and the secretion of cytokines including IL-1 beta, IL-6 and tumor necrosis factor-alpha in THP-1 cell lines by RT-PCR. Op extract significantly enhanced the proliferation of T cell clone(D10S). Transcription of cytokines including IL-1 beta, IL-6, and TNF-alpha peaked 6 hrs after exposure to Op extract(100g/ml) in the THP-1 cell line and declined and declined thereafter. In an experiment to test the dose dependency of transcription of cytokines, transcription increased at a dose of 10 g/ml and the maximum expression was obtained at 100 g/ml, 6 hrs after exposure to Op extract. These findings suggest that Op extract is a potent stimulant of immune cells including T cells and macrophages, which acts by stimulating T cell proliferation and upregulating cytokines. These phenomena imply that some edible plants may be beneficial to living animals through the activation of immune functions.

• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.200-206
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• 2014

N-(p-Coumaryol) tryptamine (CT), a phenolic amide, has been reported to exhibit anti-oxidant and anti-inflammatory activities. However, the underlying mechanism by which CT exerts its pharmacological properties has not been clearly demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of CT in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells. CT significantly inhibited LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and $PGE_2$, and protein expressions of iNOS and COX-2. In addition, CT significantly suppressed LPS-induced secretion of pro-inflammatory cytokines such as TNF-${\alpha}$ and IL-$1{\beta}$. To elucidate the underlying anti-inflammatory mechanism of CT, involvement of MAPK and Akt signaling pathways was examined. CT significantly attenuated LPS-induced activation of JNK/c-Jun, but not ERK and p38, in a concentration-dependent manner. Interestingly, CT appeared to suppress LPS-induced Akt phosphorylation. However, JNK inhibition, but not Akt inhibition, resulted in the suppression of LPS-induced responses, suggesting that JNK/c-Jun signaling pathway significantly contributes to LPS-induced inflammatory responses and that LPS-induced Akt phosphorylation might be a compensatory response to a stress condition. Taken together, the present study clearly demonstrates CT exerts anti-inflammatory activity through the suppression of JNK/c-Jun signaling pathway in LPS-challenged RAW264.7 macrophage cells.

• Toxicological Research
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• v.26 no.1
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• pp.37-46
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• 2010

This study aimed to elucidate anti-inflammatory activities from extracts of Asterina pectinifera on nitric oxide (NO) production, TNF-${\alpha}$ and IL-6 release in lipopolysaccharide (LPS)-stimulated murine macrophage cell, RAW264.7. We prepared the methanolic extracts (60-MAP, 70-MAP, 80-MAP and 90-MAP), aqueous extract (W-AP) and functional bioactive compound fraction (He-AP and EA-AP) from Asterina pectinifera according to extract method. The 60-MAP, 70-MAP, 80-MAP, 90-MAP and W-AP were significantly suppressed LPS-induced production NO, TNF-${\alpha}$ and IL-6 secretion in a concentration-dependent manner (P < 0.05). Especially, 80-MAP by extracted 80% methanol had the strongest activity in reduction of inflammatory mediators among these extracts. Indeed, to identify active fraction, which contained potential bioactive compounds, from 80-MAP of Asterina pectinifera, we tested anti-inflammatory activity of the He-AP or the EA-AP. The He-AP was next extracted from 80-MAP and the EA-AP were extracted from the other methanol layer except the He-AP. The EA-AP demonstrated a strong anti-inflammatory effect through its ability to reduce NO production and it also inhibited the production of proinflammatory cytokines such as IL-6 and TNF-${\alpha}$ at low concentration. These results suggested that the methanolic extract from Asterina pectinifera had the potential inhibitory effects on the production of these inflammatory mediators.

• Journal of the Korea Society of Computer and Information
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• v.27 no.1
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• pp.175-181
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• 2022

In this study, we tested the anti-inflammatory effects of broccoli leaf hexane fraction to confirm the applicability as a functional material in food and cosmetics. This sample was extracted using 70% ethanol from Broccoli leaf and then fractionated with hexane. The production of pro-inflammatory cytokines (TNF-α, IL-4, IL-6, IL-1β), protein expression of iNOS and COX-2, phosphorylation of MAPKs (ERK, JNK, p38) and NF-κB with broccoli leaf hexane fraction were assayed on LPS-stimulated RAW264.7 cells. The broccoli leaf hexane fraction inhibited the secretion of pro-inflammatory cytokines and protein expression of iNOS and COX-2. Also, the broccoli leaf hexane fraction reduced the phosphorylation of MAPKs and NF-κB. Therefore, it is considered that th broccoli leaf hexane fraction has the potential to be used as a natural anti-inflammatory material in food and cosmetics. In the future, it is considered necessary to study the anti-inflammatory mechanism and identification of major bioactive substances.

• BMB Reports
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• v.54 no.5
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• pp.260-265
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• 2021

Dysregulation of inflammation induced by noninfectious stress conditions, such as nutrient deprivation, causes tissue damage and intestinal permeability, resulting in the development of inflammatory bowel diseases. We studied the effect of autophagy on cytokine secretion related to intestinal permeability under nutrient deprivation. Autophagy removes NLRP3 inflammasomes via ubiquitin-mediated degradation under starvation. When autophagy was inhibited, starvation-induced NLRP3 inflammasomes and their product, IL-1β, were significantly enhanced. A prolonged nutrient deprivation resulted in an increased epithelial mesenchymal transition (EMT), leading to intestinal permeability. Under nutrient deprivation, IL-17E/25, which is secreted by IL-1β, demolished the intestinal epithelial barrier. Our results suggest that an upregulation of autophagy maintains the intestinal barrier by suppressing the activation of NLRP3 inflammasomes and the release of their products, including pro-inflammatory cytokines IL-1β and IL-17E/25, under nutrient deprivation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.9
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• pp.1053-1060
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• 2017

The present study examined the anti-inflammatory and anti-oxidative effects of Pinus koraiensis (PK) cone shell extracts in vitro. Anti-inflammatory and anti-oxidative effects of PK cone shell extracted with hot water, 20% ethanol (EtOH), or 50% EtOH were examined using 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) radical scavenging assay, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activites, as well as nitric oxide (NO) and anti-inflammatory cytokine measurements. The 20% EtOH extract of the PK cone shell decreased the NO and inflammatory cytokines secretion, and increased the ABTS radical scavenging, SOD, CAT, and GPx activities. This indicates that the 20% EtOH extract of the PK cone shell would be helpful in inflammation and oxidation systems. Therefore, the 20% EtOH extract of PK cone shell has great potential as a useful health food.

• Korean Journal of Food Science and Technology
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• v.53 no.3
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• pp.344-347
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• 2021

In this study, the hepatotoxic mechanism of chaparral (Larrea tridentata) was investigated through in vitro experiments that measured cell death, inflammatory cytokine secretion, and intracellular fat accumulation by treating HepG2 hepatocytes with a 70% ethanol extract of chaparral at concentrations ranging from 0.001 to 100 ㎍/mL. Cell death was observed after treatment with chaparral extract at concentrations of 1-100 ㎍/mL (p<0.05). The secretion of the inflammatory cytokines, interleukin-8 and macrophage-colony stimulating factor, and fat accumulation were significantly increased even at a concentration of 0.1 ㎍/mL, which was 10 times lower than the observed concentration resulting in cell death (p<0.05). Hepatitis caused by inflammatory cytokine secretion and fat accumulation was shown to be a form of hepatotoxicity induced by chaparral extract. Hepatitis was expressed at a concentration lower than that causing serious toxicity such as cell death, suggesting that hepatotoxicity, including hepatitis, may be caused by ingestion of low concentrations of chaparral.

• IMMUNE NETWORK
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• v.11 no.3
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• pp.169-174
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• 2011

Background: NADPH oxidase (NOX) modulates cell proliferation, differentiation and immune response through generation of reactive oxygen species. Particularly, NOX2 is recently reported to be important for regulating Treg cell differentiation of CD4+ T cells. Methods: We employed ovalbumin-induced airway inflammation in wild-type and NOX2-deficient mice and analyzed tissue histopathology and cytokine profiles. Results: We investigated whether NOX2-deficiency affects T cell-mediated airway inflammation. Ovalbumin injection which activates T cell-mediated allergic response increased airway inflammation in wild-type mice, as evidenced by increased immune cell infiltration, allergic cytokine expression, and goblet cell hyperplasia in the lung. Interestingly, NOX2 knockout (KO) mice were more susceptible to allergen-induced lung inflammation compared to wild-type mice. Immune cells including neutrophils, lymphocytes, macrophages, and eosinophils were drastically infiltrated into the lung of NOX2 KO mice and mucus secretion was substantially increased in deficiency of NOX2. Furthermore, inflammatory allergic cytokines and eotaxin were significantly elevated in NOX2 KO mice, in accordance with enhanced generation of inflammatory cytokines interleukin-17 and interferon-${\gamma}$ by CD4+ T cells. Conclusion: These results indicate that NOX2 deficiency favorably produces inflammatory cytokines by T cells and thus increases the susceptibility to severe airway inflammation.

• Journal of Ginseng Research
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• v.33 no.2
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• pp.149-154
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• 2009

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and progressive cartilage and bone erosion. Korean red ginseng (KRG) has been shown to have an anti-inflammatory effect by inhibiting the secretion of inflammatory cytokines like $TNF-{\alpha}$, IL-1, -6, and -8, and $IPN-{\gamma}$. In this study, whether KRG extract has an inhibitory effect on the collagen-inducible development of arthritis in DBA/1J mice was investigated. To induce arthritis, type II collagen emulsified in Complete Freund's Adjuvant was intradermally injected into the base of the tails of mice. Three weeks after the initial injection, a booster injection of type II collagen emulsified in Incomplete Freund's Adjuvant was administered. The oral administration of KRG extract for 8${\sim}$10 weeks at the dose of 300 mg/kg (three days a week) inhibited the development of arthritis in the experimental group, compared to the control group which was given saline. While the administration of KRG extract three times a week demonstrated both preventive and inhibitory effects, the administration of KRG extract once a week had little inhibitory effect. In other studies, the regimen of KRG administration has been shown to decrease the plasma level of inflammatory cytokines like IL-8 and TNF-${\alpha}$, but the plasma levels of these cytokines were not decreased in the present study. The results of the present study suggest that KRG has preventive and inhibitory effects on collagen-induced arthritis.