• The Korean Journal of Physiology and Pharmacology
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• v.19 no.2
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• pp.183-189
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• 2015

Foeniculum vulgare Mill. (fennel) is used to flavor food, in cosmetics, as an antioxidant, and to treat microbial, diabetic and common inflammation. No study to date, however, has assessed the anti-inflammatory effects of fennel in experimental models of inflammation. The aims of this study were to investigate the anti-inflammatory effects of fennel in model of lipopolysaccharide (LPS)-induced acute lung injury. Mice were randomly assigned to seven groups (n=7~10). In five groups, the mice were intraperitoneally injected with 1% Tween 80-saline (vehicle), fennel (125, 250, $500{\mu}l/kg$), or dexamethasone (1 mg/kg), followed 1 h later by intratracheal instillation of LPS (1.5 mg/kg). In two groups, the mice were intraperitoneally injected with vehicle or fennel ($250{\mu}l/kg$), followed 1 h later by intratracheal instillation of sterile saline. Mice were sacrificed 4 h later, and bronchoalveolar lavage fluid (BALF) and lung tissues were obtained. Fennel significantly and dose-dependently reduced LDH activity and immune cell numbers in LPS treated mice. In addition fennel effectively suppressed the LPS-induced increases in the production of the inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, with $500{\mu}l/kg$ fennel showing maximal reduction. Fennel also significantly and dose-dependently reduced the activity of the proinflammatory mediator matrix metalloproteinase 9 and the immune modulator nitric oxide (NO). Assessments of the involvement of the MAPK signaling pathway showed that fennel significantly decreased the LPS-induced phosphorylation of ERK. Fennel effectively blocked the inflammatory processes induced by LPS, by regulating pro-inflammatory cytokine production, transcription factors, and NO.

• Food Science of Animal Resources
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• v.34 no.5
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• pp.630-637
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• 2014

We previously demonstrated that water-soluble egg yolk extract is not related to elevation of serum immunoglobulin E, which can initiate allergic reactions; however, it increases the level of high density lipoprotein (HDL)-cholesterol and the activity of B lymphocytes. In this study, egg white (EW) was fed to BALB/c mice to determine its influence on growth efficiency, immune modulation, and changes in serum lipid levels. A total of 50 five-wk-old BALB/c male mice were divided into 5 groups, 4 of which were fed 0, 10, 50, or 100 mg/d EW for 4 wk. Mice with an uptake of 10, 50 and 100 mg/d EW showed no significant changes in daily weight gain, feed efficiency rate, or populations of white blood cells. However, the activities of both B and T lymphocytes were significantly increased in all three EW groups at the final week of treatment. Interestingly, serum levels immunoglobulin E were not altered by EW consumption, but the IgG level was significantly increased in the 100 mg/d EW group. Serum lipid profile analyses showed no significant changes in total cholesterol, HDL, low density lipoprotein, or triglyceride levels by EW consumption. Taken together, these data demonstrate that consumption of EW promotes immune cell activities and the upregulation of serum IgG levels. However, we found no changes in serum lipid profiles and IgE levels. Therefore, our study suggests that consumption of EW might not be related to the risk of food allergy, but could be an excellent candidate for the maintenance of physiological homeostasis.

• Food Science of Animal Resources
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• v.35 no.3
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• pp.398-405
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• 2015

Egg allergy has been shown to be the most common food allergy in children with atopic dermatitis. Allergic reactions to proteins derived from egg white (EW) are more common than those derived from egg yolk. Ovomucoid, ovalbumin, ovotransferrin, and lysozyme have been identified as major allergens in EW. This study was conducted to evaluate the effect of EW on immune modulation in an induced allergy mouse model. A total of 50 five-week-old BALB/c male mice were treated with trimellitic anhydride (TMA) for three weeks to induce allergy-like symptoms. The TMA-treated mice were rested for one week and then divided into five groups and fed 0, 10, 50, and 100 mg/d EW for four weeks. All EW consumption groups showed no significant increase or decrease in the populations of white blood cells; however, a significant increase in B-lymphocyte activity was observed in the fourth week. Furthermore, EW consumption did not influence serum immunoglobulin G and immunoglobulin E levels. Taken together, these data demonstrate that the consumption of EW by TMA-treated mice did not increase allergic parameters such as serum IgE level, but enhanced the lymphocyte activities against pathogens. Therefore, this study suggests that the consumption of EW promotes Th2 immune modulation, and EW could be an excellent candidate for maintaining health.

• IMMUNE NETWORK
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• v.11 no.2
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• pp.123-133
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• 2011

Background: Mycobacterium tuberculosis (Mtb) heparin binding hemagglutinin (HBHA) is an Ag known to evoke effective host immune responses during tuberculosis infection. However, the molecular basis of the host immune response to HBHA has not been fully characterized. In this study, we examined the molecular mechanisms by which HBHA can induce the expression of proinflammatory cytokines in macrophages. Methods: HBHA-induced mRNA and protein levels of proinflammatory cytokines were determined in bone marrow-derived macrophages (BMDMs) using RT-PCR and ELISA analysis. The roles of intracellular signaling pathways for NF-${\kappa}B$, PI3-K/Akt, and MAPKs were investigated in macrophage proinflammatory responses after stimulation with HBHA. Results: HBHA robustly activated the expression of mRNA and protein of both TNF-${\alpha}$ and IL-6, and induced phosphorylation of NF-${\kappa}B$, Akt, and MAPKs in BMDMs. Both TNF-${\alpha}$ and IL-6 production by HBHA was regulated by the NF-${\kappa}B$, PI3-K, and MAPK pathways. Furthermore, PI3-K activity was required for the HBHA-induced activation of ERK1/2 and p38 MAPK, but not JNK, pathways. Conclusion: These data suggest that mycobacterial HBHA significantly induces proinflammatory responses through crosstalk between the PI3-K and MAPK pathways in macrophages.

• The Korean Journal of Food And Nutrition
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• v.34 no.2
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• pp.196-206
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• 2021

The main purpose of this study was to examine the correlation between the consumption of red ginseng-based 'SSR' for 30 days and the reduction in human fatigue, blood component changes, and immune cell activity in 35 human subjects. 'SSR' is composed of zinc oxide, folic acid, and D-α-tocopherol with red ginseng as the main component. According to the protocol criteria of the study, 35 subjects who understood the purpose of the study and signed an informed consent form were selected. The fatigue survey was conducted through a questionnaire, and after taking 'SSR', a decreased tendency of physical, mental, and neurosensory fatigue was observed. In hematological analysis, no significant changes were observed in the levels of WBC, RBC, and hemoglobin; however, AST (SGOT) and ALT (SGPT) levels were statistically significantly decreased. In immunological analysis, it was observed that the proliferative effect of T cells (CD3+CD4+) was greater than that of NK cells (CD16+CD56+). The collected data were subjected to t-test analysis using the SPSS 25.0 statistical program. The result from this study proposes that 'SSR' can be used as a functional food material as it reduces human fatigue and enhances immune function.

• Korean Journal of Plant Resources
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• v.36 no.4
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• pp.257-263
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• 2023

Autophagy contributes to enhancing the immune system (innate and adaptive immune system) against foreign pathogens. Autophagy of macrophages is used as a major indicator for developing vaccine adjuvants to increase the adaptive immune response. In this study, water extracts from Rosa acicularis leaves (RAL) increased the production of immunostimulatory mediators and phagocytic activity in RAW264.7 cells. RAL increased p62/SQSTM1 expression. Inhibition of TLR4, JNK, and PI3K/AKT blocked RAL-mediated increase of p62/SQSTM1. RAL activated JNK and PI3K/AKT signaling. RAL-mediated activations of JNK and PI3K/AKT signaling were reversed by TLR4 inhibition. Taken together, it is believed that RAL-mediated autophagy may be dependent on activating via TLR4-dependent activation of JNK and PI3K/AKT signaling in macrophages.

• BMB Reports
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• v.42 no.7
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• pp.421-426
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• 2009

Glucocorticoids regulate multiple physiological processes such as metabolic homeostasis and immune response. Mouse Pon2 (mPon2) acts as an antioxidant to reduce cellular oxidative stress in cells. In this present study, we investigated the transcriptional regulation of mPon2 by glucocorticoids. In the presence of glucocorticoid analogue dexamethasone, the expression of mPon2 mRNA in cells was increased, whereas the expression was inhibited by a transcription inhibitor actinomycin D. Glucocorticoid receptors bound to the putative glucocorticoid response elements located between -593 bp and -575 bp of the mPon2 promoter. Transcriptional activity was completely blocked when the putative element was mutated. Taken together, these results suggest that the expression of the mPon2 gene is directly regulated by glucocorticoid-glucocorticoid receptor complexes.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.609-617
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• 2013

Renal cell carcinomas make up 3% of all cancers and one in four patients is metastatic at time of diagnosis. This cancer is one of the most resistant to cytotoxic chemotherapy. Studies have shown that the efficiency of interferon-alpha and/or interleukin-2 based immune therapies is limited in patients with metastatic renal cell carcinoma but latest advances in molecular biology and genetic science have resulted in better understanding of its biology. Tumor angiogenesis, tumor proliferation and metastasis develop by the activation of signal message pathways playing a role in the development of renal cell carcinomas. Better definition of these pathways has caused an increase in preclinic and clinical studies into target directed treatment of renal cell carcinoma. Many recent studies have shown that numerous anti-angiogenic agents have marked clinical activity. In this article, the focus is on general characteristics of molecular pathways playing a major role in renal cell carcinoma, reviewing clinical information onagents used in the target directed treatment of metastatic lesions.

• Journal of Microbiology and Biotechnology
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• v.28 no.6
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• pp.874-882
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• 2018

Curcumin is known to possess various biological functions, including anti-inflammatory, anti-oxidative, and anti-cancer activities. Natural killer (NK) cells are large lymphocytes that directly kill cancer cells. However, many aggressive cancers, including breast cancer, were reported to escape the successful killing of NK cells in a tumor microenvironment. In this study, we investigated the anti-cancer effect of curcumin in coculture of human breast carcinoma MDA-MB-231 and NK (NK-92) cells. We found that curcumin had an immune-stimulatory effect on NK-92 by increasing the surface expression of the $CD16^+$ and $CD56^{dim}$ population of NK-92. We confirmed that the cytotoxic effect of NK-92 on MDA-MB-231 was significantly enhanced in the presence of curcumin, which was highly associated with the activation of Stat4 and Stat5 proteins in NK-92. Finally, this improved anticancer effect of curcumin was correlated with decreased expression of pErk and PI3K in MDA-MB-231.

• Biomedical Science Letters
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• v.24 no.4
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• pp.305-310
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• 2018

Microglia are emerging as critical regulators of innate immune responses in AD and other neurodegenerative disorders, highlighting the importance of understanding their molecular and cellular mechanisms. We attempted to determine the role of crosstalk signaling between $IFN-{\gamma}$ and $TGF-{\beta}$ in $A{\beta}$ clearance by microglia cells. We used in vitro and in vivo mouse models that recapitulated acute and chronic aspects of microglial responses to $A{\beta}$ peptides. We showed that crosstalk signaling between $TGF-{\beta}$ and Smad2 was an important mediator of neuro-inflammation. These findings suggest that microglial $TGF-{\beta}$ activity enhances the pathological progression to AD. As $TGF-{\beta}$ displays broad regulatory effects on beneficial microglial functions, the activation of inflammatory crosstalk signaling between $TGF-{\beta}$ and Smad2 may be a promising strategy to restore microglial functions, halt the progression of $A{\beta}$-driven pathology, and prevent AD development.