• Journal of Haehwa Medicine
• /
• v.15 no.2
• /
• pp.121-134
• /
• 2006

This study saw the anti-allergy effect by the immunity regulation action of Yanghyelyoonbotang (YHYBT) consists 12 kinds of herbal medicine agents. Consequently, YHYBT controlled the amount of secretion of various infla- mmatory cytokines, chemokine, monocyte chemotactic protein and histamine from cells (HMC-1, THP-1, EoL-1) stimulated by PMA, A23187 or HDM. 1. YHYBT did not show cytotoxicity on cultured human fibroblast cells under 250 ${\mu}g/m\ell$ concentration. 2. YHYBT suppressed IL-8, TNF-$\alpha$, IL-6 mRNA expression in the HMC-1 cell stimulated with PMA and A23187. 3. YHYBT significantly suppressed IL-6 release in the THP-1 and EoL-1 cell stimulated with HDM. 4. YHYBT significantly suppressed histamine release in the HMC-1 cell stimulated with PMA and A23187 in a dose-dependent. 5. YHYBT significantly suppressed $\beta$-Hexosaminidase release in the HMC-1 cell stimulated with A23187 in a dose-dependent. 6. YHYBT suppressed NF-$\kappa$B gene expression in the RBL-2H3 cell stimulated with PMA in a dose-dependent. These results suggested that YHYBT has suppressive effects on allergic reaction and pro-inflammatory cytokines in various cell lines through the regulation of immune system. YHYBT has potential to use as an antiallergic agents.

• Journal of Haehwa Medicine
• /
• v.15 no.2
• /
• pp.135-148
• /
• 2006

Sophorae Radix (SFR) is known as a therapeutic drug that has been used in Oriental traditional medicine for the treatment of skin and mucosal ulcers, gastrointestinal hemorrhage, diarrhea, inflammation and arrhythmia. In the present study, we examined the effects of the aqueous extract of SFR on anti-inflammation, anti-allergic and anti-oxidant effect in various cell lines; they include mouse lung fibroblast cells (hFCs), human mast cells (HMC-1), human monocytic cells (THP-1), and RAW 264.7 cells. Treatment with SFR extract at a concentration of 250 ${\mu}g$/ml for 24h showed no significant decrease in the survival rate of the hFCs. SFR decreased the mRNA expression of IL-8, TNF-$\alpha$, and IL-6 in HMC-1 cells. SFR extract treatment significantly inhi-bited the protein expression of IL-6 and, IL-8 induced by mite in THP-1 cells and it also did MCP-1 expression. We examined the alternation of histamine release in HMC-1 cells for investigating anti-allergic effect of SFR. Histamine secretion decreased after the treatment with SFR. In addition, SFR extract treatment at a concentration of 10 ${\mu}g$/ml, 100 ${\mu}g$ /ml, and 200 ${\mu}g$/ml lowered the $\beta$-hexosaminidase to 10.3%, 21.7%, and 50.8%, respectively. IC50 of SFR extract in RBL-2H3 cells was 196.85 ${\mu}g$/ml. Both activity of NF-$\kappa$B promoter in RBL-2H3 cells significantly diminished after the dose-dependent treatment of SFR. Therefore, our results indicate that SFR has anti-inflammatory and it may be useful for treating allergic diseases such as atopic dermatitis.

• Journal of Ginseng Research
• /
• v.41 no.2
• /
• pp.188-194
• /
• 2017

Background: Fermented black ginseng (FBG) is processed ginseng by the repeated heat treatment and fermentation of raw ginseng. The protective effect and mechanism of FBG on cisplatin-induced nephrotoxicity was investigated to evaluate its therapeutic potential. Methods: The free radical scavenging activity of FBG was measured using 1,1-diphenyl-2-picrylhydrazyl (DPPH). In addition, the protective effect against cisplatin-induced renal damage was tested in rats. FBG was orally administered every day at a dose of 150 mg/kg body weight for 10 d, and a single dose of cisplatin was administered intraperitoneally (7.5 mg/kg body weight) with 0.9% saline on the $4^{th}$ d. Results: The DPPH radical-scavenging activity of FBG ($IC_{50}=384{\mu}g/mL$) was stronger than that of raw ginseng. The improved DPPH radical-scavenging activity was mediated by the generation phenolic compounds. The decreased cell viability by cisplatin was recovered significantly after treatment with FBG in a dose-dependent manner. Then, the protective effect of FBG on cisplatin-induced oxidative renal damage was investigated in rats. The decreased creatinine clearance levels, which are a reliable marker for renal dysfunction in cisplatin-treated rats, were reduced to the normal level after the administration of FBG. Moreover, FBG showed protective effects against cisplatin-induced oxidative renal damage in rats through the inhibition of $NF-{\kappa}B/p65$, COX-2, and caspase-3 activation. Conclusion: These results collectively show that the therapeutic evidence for FBG ameliorates the nephrotoxicity via regulating oxidative stress, inflammation, and apoptosis.

• Journal of the korean academy of Pediatric Dentistry
• /
• v.42 no.2
• /
• pp.180-187
• /
• 2015

Incontinentia pigmenti, also called Bloch-Sulzberger syndrome, is a rare X-linked inherited dominant disorder that affects females, but causes spontaneous abortion of prenatal males. Incontinentia pigmenti is a systemic disease with clinical features similar to ectodermal dysplasia, including congenitally missing teeth. The pathogenesis is related to gene mutations in NF-kappa-B essential modulator on chromosome Xq28. Incontinentia pigmenti is caused by a defect in the developmental stage of organs originating from the ectoderm or mesoderm and involves the skin, eyes, hair, teeth and central nervous system. This report discusses the management of three cases of 3 to 5 years old females with incontinentia pigmenti and accompanying multiple missing teeth. The cases had sparse hair, and showed oligodontia and anomalous crowns with supplementary cusps in the posterior teeth and conical anterior teeth. Removable space maintainers were applied, achieving improved esthetics, recovery of mastication and increased self-esteem in the patients.

• Biomedical Science Letters
• /
• v.24 no.3
• /
• pp.213-220
• /
• 2018

Triglyceride (TG) is known to be associated with inflammatory disease including atherosclerosis. In a variety of atherosclerosis models, T lymphocytes are localized in the earliest lesions of atherosclerosis. T cell associated cytokines such as $TNF-{\alpha}$ and $IFN-{\gamma}$ have pre-dominant inflammatory effects in chronic vascular diseases. In our previous study, we found that the expression of $TNF-{\alpha}$ and its receptor, $TNF-{\alpha}R$ was increased when Jurkat T lymphocyte cell lines were exposed to TGs. Therefore, experiments were conducted to determine which cell signaling pathway are involved in the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs. To identify signal transduction pathways involved in TG-induced upregulation of $TNF-{\alpha}$, we treated TG-exposed Jurkat T cells with specific inhibitors for MEK1, PI3K, $NF-{\kappa}B$ and PKC. We found that inhibition of the MEK1 pathway blocked TG-induced upregulation of $TNF-{\alpha}$. However, the expression level of $TNF-{\alpha}R$ did not change with any signal transduction inhibitor. Based on this observation, we suggest that increase of exogenous TG induces increase of $TNF-{\alpha}$ expression through MEK1 pathway in Jurkat T cells. In addition, it was confirmed that the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs occurs via different pathways.

• Journal of Ginseng Research
• /
• v.39 no.4
• /
• pp.376-383
• /
• 2015

Background: Panax ginseng has a wide range of biological activities including anti-inflammatory, antioxidant, and immunomodulatory functions. Wild ginseng cambial meristematic cells (CMCs) were obtained from P. ginseng cambium. This study examined the protective mechanism of wild ginseng CMCs against $\small{D}$-galactosamine (GalN)-induced liver injury. GalN, a well-known hepatotoxicant, causes severe hepatocellular inflammatory damage and clinical features similar to those of human viral hepatitis in experimental animals. Methods: Hepatotoxicity was induced in rats using GalN (700 mg/kg, i.p.). Wild ginseng CMCs was administered orally once a day for 2 wks, and then 2 h prior to and 6 h after GalN injection. Results: Wild ginseng CMCs attenuated the increase in serum aminotransferase activity that occurs 24 h after GalN injection. Wild ginseng CMCs also attenuated the GalN-induced increase in serum tumor necrosis factor-${\alpha}$, interleukin-6 level, and hepatic cyclooxygenase-2 protein and mRNA expression. Wild ginseng CMCs augmented the increase in serum interleukin -10 and hepatic heme oxygenase-1 protein and mRNA expression that was induced by GalN, inhibited the increase in the nuclear level of nuclear factor-kappa B, and enhanced the increase in NF-E2-related factor 2. Conclusion: Our findings suggest that wild ginseng CMCs protects liver against GalN-induced inflammation by suppressing proinflammatory mediators and enhancing production of anti-inflammatory mediators.

• Journal of Ginseng Research
• /
• v.36 no.4
• /
• pp.375-382
• /
• 2012

Ginsenoside Rp1 (G-Rp1) is a saponin derivate that provides anti-metastatic activities through inhibition of the NF-${\kappa}B$ pathway. In this study, we examined the effects of G-Rp1 on regulatory T cell (Treg) activation. After treatment of splenocytes with G-Rp1, Tregs exhibited upregulation of IL-10 expression, and along with dendritic cells (DCs), these Tregs showed increased cell number compared to other cell populations. The effect of G-Rp1 on Treg number was augmented in the presence of lipopolysaccharide (LPS), which mimics pathological changes that occur during inflammation. However, depletion of DCs prevented the increase in Treg number in the presence of G-Rp1 and/or LPS. In addition, G-Rp1 promoted the differentiation of the memory types of $CD4^+Foxp3^+CD62L^{low}$ Tregs rather than the generation of new Tregs. In vivo experiments also demonstrated that Tregs and DCs from mice that were fed G-Rp1 for 7 d and then injected with LPS exhibited increased activation compared with those from mice that were injected with LPS alone. Expression of TGF-${\beta}$ and CTLA4 in Tregs was increased, and upregulation of IL-2 and CD80/CD86 expression by DCs affected the suppressive function of Tregs through IL-2 receptors and CTLA4. These data demonstrate that G-Rp1 exerts anti-inflammatory effects by activating Tregs in vitro and in vivo.

• Journal of Ginseng Research
• /
• v.33 no.2
• /
• pp.93-98
• /
• 2009

To understand the anti-allergic mechanism of compound K, which is a metabolite of ginsenoside Rb1, a main constituent of the root of Panax ginseng C.A. Meyer (family Araliaceae), its inhibitory effect against IgE-antigen complex IAC)-induced passive cutaneous anaphylaxis (PCA) reaction in mice and mRNA and protein expressions of allergic cytokines in lAC-stimulated RBL-2H3 cells were investigated. Orally administered ginsenoside Rb1 more potently inhibited PCA reaction when administered at 5 h prior to the lAC treatment than when administered at I h before. However, compound K orally administered 1 h before lAC treatment showed a more potent anti-PCA reaction effect than when treated at 5 h before. Orally administered ginsenoside Rb1 more potently inhibited PCA reaction induced by lAC in mice than intraperitoneally treated one, apart from orally administered its metabolite, compound K, which was more potent than the orally administered one. The compound K, a metabolite of ginsenoside Rb1, inhibited mRNA and protein expressions of IL-4 and TNF-${\alpha}$ and the activation of their transcription factor NF-$\kappa$B and MAPK in lAC-stimulated RBL-2H3 cells. These findings suggest that orally administered ginsenoside Rb1 may be dependent on its metabolism by intestinal microflora in the intestine and the compound K may improve allergic diseases by the inhibition of IL-4 and TNF-${\alpha}$ expresseion.

• IMMUNE NETWORK
• /
• v.14 no.6
• /
• pp.296-306
• /
• 2014

There is growing evidence that crosstalk between mantle cell lymphoma (MCL) cells and stromal microenvironments, such as bone marrow and secondary lymphoid tissues, promotes tumor progression by enhancing survival and growth as well as drug resistance of MCL cells. Recent advances in the understanding of lymphoma microenvironment have led to the identification of crucial factors involved in the crosstalk and subsequent generation of their targeted agents. In the present study, we evaluated the combinatory effect of blocking antibodies (Ab) targeting CXCR4 and VLA-4, both of which were known to play significant roles in the induction of environment-mediated drug resistance (EMDR) in MCL cell line, Jeko-1. Simultaneous treatment with anti-CXCR4 and anti-VLA-4 Ab not only reduced the migration of Jeko-1 cells into the protective stromal cells, but also enhanced sensitivity of Jeko-1 to a chemotherapeutic agent to a greater degree than with either Ab alone. These combinatorial effects were associated with decreased phosphorylation of ERK1/2, AKT and NF-${\kappa}B$. Importantly, drug resistance could not be overcome once the adhesion of Jeko-1 to the stromal occurred despite the combined use of Abs, suggesting that the efforts to mitigate migration of MCLs should be attempted as much as possible. Our results provide a basis for a future development of therapeutic strategies targeting both CXCR4 and VLA-4, such as Ab combinations or bispecific antibodies, to improve treatment outcomes of MCL with grave prognosis.

• Molecules and Cells
• /
• v.27 no.2
• /
• pp.251-255
• /
• 2009

Sepsis is the leading cause of death in critically ill patients. Today, around 60% of all cases of sepsis are caused by Gram-negative bacteria. The cell wall component lipopolysaccharide (LPS) is the main initiator of the cascade of cellular reactions in Gram-negative infections. The core receptors for LPS are toll-like receptor 4 (TLR4), MD-2 and CD14. Attempts have been made to antagonize the toxic effect of endotoxin using monoclonal antibodies against CD14 and synthetic lipopolysaccharides but there is as yet no effective treatment for septic syndrome. Here, we describe an inhibitory effect of a phosphatidylethanolamine derivative, PE-DTPA (phosphatidylethanolamine diethylenetriaminepentaacetate) on LPS recognition. PE-DTPA bound strongly to CD14 ($K_d$, $9.52{\times}10^{-8}M$). It dose dependently inhibited LPS-mediated activation of human myeloid cells, mouse macrophage cells and human whole blood as measured by the production of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and nitric oxide, whereas other phospho-lipids including phosphatidylserine and phosphatidylethanolamine had little effect. PE-DTPA also inhibited transcription dependent on $NF-{\kappa}B$ activation when it was added together with LPS, and it rescued LPS-primed mice from septic death. These results suggest that PE-DTPA is a potent antagonist of LPS, and that it acts by competing for binding to CD14.