• IMMUNE NETWORK
• /
• v.13 no.6
• /
• pp.283-288
• /
• 2013

The pro-inflammatory cytokines tumor necrosis factor-${\alpha}$ (TNF${\alpha}$) and interleukin (IL)-$1{\beta}$ are crucial mediators involved in chronic inflammatory diseases. Inflammatory signal pathways regulate inflammatory cytokine expression-mediated by p38 mitogen activated protein kinase (p38MAPK). Therefore, considerable attention has been given to p38MAPK as a target molecule for the development of a novel anti-inflammatory therapeutics. BIRB 796, one of p38MAPK inhibitor, is a candidate of therapeutic drug for chronic inflammatory diseases. In this study, we investigated the effect of BIRB 796 on inflammatory cytokine productions by lipopolysaccharide (LPS) in different immune cell types. BIRB 796 reduced LPS-mediated IL-8 production in THP-1 cells but not in Raw 264.7 cells. Further analysis of signal molecules by western blot revealed that BIRB 796 sufficiently suppressed LPS-mediated phosphorylation of p38MAPK in both cell types whereas it failed to block inhibitor of kappa B (I-${\kappa}B$) degradation in Raw 264.7 cells. Taken together, these results suggest that the anti-inflammatory function of BIRB 796 depends on cell types.

• The Bulletin of The Korean Astronomical Society
• /
• v.41 no.1
• /
• pp.68.2-68.2
• /
• 2016

We present the variability and time lag measurements of PG 0934+013 based on the photometric and spectroscopic monitoring campaign over two years. We obtained 46 epochs of data from the spectroscopic campaign, which was carried out using the South African Large Telescope with 1 week cadence over two sets of 4 month-long observing period, while we obtained 80 epochs of B band data from the campaign. Due to the six month gap between two campaigns, we separately measured the time lag of the $H{\beta}$ emission line by comparing the emission line light curve with the B band continuum light curve using the cross-correlation function techniques. We determined the time lags and black hole mass.

• 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.

• Archives of Pharmacal Research
• /
• v.29 no.5
• /
• pp.424-429
• /
• 2006

In the present study, a human mammary epithelial cell (HMEC) culture model was developed to evaluate the potential involvement of carrier-mediated transport systems in drug transfer into milk. Trypsin-resistant HMECs were seeded on $Matrigel^{circledR}-coated$ filters to develop monolayers of functionally differentiated HMEC. Expression of the specific function of HMEC monolayers was dependent of the number of trypsin treatments. Among the monolayers with different numbers of treatment (treated 1 to 3 times), the monolayer treated 3 times (3-t-HMEC monolayer) showed the highest maximal transepithelial resistance and expression of $\beta-casein$ mRNA as an index of differentiation. Transport of tetraethylammonium (TEA) across the 3-t-HMEC monolayer in the basolateral-to-apical direction was significantly higher than that in the apical-to-basolateral direction (p<0.05), whereas such directionality was not observed for p-aminohippurate, suggesting the existence of organic cation transporters, but not organic anion transporters. In fact, expression of mRNAs of human organic cation transporter (OCT) 1 and 3 were detected in the 3-t-HMEC monolayer. These results indicate that the 3-t-HMEC monolayer is potentially useful for the evaluation of carrier-mediated secretion of drugs including organic cations into human milk.

• Biomaterials and Biomechanics in Bioengineering
• /
• v.3 no.1
• /
• pp.37-46
• /
• 2016

To maintain activity in a coenzyme/enzyme mixture system, such as ${\beta}$-nicotinamide adenine dinucleotide (NADH)/dehydrogenase, the water-soluble 2-methacryloyloxyethyl phosphorylcholine (MPC) polymers as an additive were synthesized and investigated for their stabilizing function. The inhibitor for the NADH/dehydrogenase reaction was spontaneously formed when the NADH was stored in the dehydrogenase solution. Therefore, we hypothesized that if the additive polymer could interact with an inhibitor without any adverse effect on the dehydrogenase, the activity in the NADH/dehydrogenase mixture could be maintained. We selected lactose dehydrogenase (LDH) as the enzyme, and the NADH was dissolved and incubated at $37^{\circ}C$ in the LDH solution containing the polymers. The phospholipid polymers used in this study were poly(MPC) (PMPC), poly(MPC-co-3-trimethylammonium-2-hydroxypropyl methacrylate chloride) (PMQ) and poly[MPC-co-potassium 3-methacryloyloxypropyl sulfonate ($MSO_3$)] ($PMMSO_3$). The poly($MSO_3$) was used as a reference. For the PMQ and $PMSO_3$ aqueous solutions, the activity of the NADH/LDH mixture system decreased with incubation time as the same level or lower than that in the Tris buffered solution in the absence of the polymers. However, for the poly($MPC-co-MSO_3$) ($PMMSO_3$) aqueous solution, the activity of the NADH/LDH mixed system was six times higher than that in the buffered solution even after a 3-days incubation. The LDH activity was 1.5-1.8 times higher in the presence of the $PMMSO_3$ compared with that in the $PMSO_3$ solution. The mixture of two polymers, poly(MPC) and poly($MSO_3$), did not produce any stabilization. Thus, both the MPC and $MSO_3$ units in the polymer chain had important and cooperative effects for stabilizing the NADH/LDH mixture.

• Animal cells and systems
• /
• v.16 no.4
• /
• pp.302-312
• /
• 2012

The purpose of this study was to examine whether Phellodendri Cortex extract (PCE) could improve learning and memory impairments caused by lipopolysaccharide (LPS)-induced inflammation in the rat brain. The effect of PCE on modulating pro-inflammatory mediators in the hippocampus and its underlying mechanism were investigated. Injection of LPS into the lateral ventricle caused acute regional inflammation and subsequent deficits in spatial learning ability in the rats. Daily administration of PCE (50, 100, and 200 mg/kg, i.p.) for 21 days markedly improved the LPS-induced learning and memory disabilities in the Morris water maze and passive avoidance test. PCE administration significantly decreased the expression of pro-inflammatory mediators such as tumor necrosis factor-${\alpha}$, interleukin-$1{\beta}$, and cyclooxygenase-2 mRNA in the hippocampus, as assessed by RT-PCR analysis and immunohistochemistry. Together, these findings suggest that PCE significantly attenuated LPS-induced spatial cognitive impairment through inhibiting the expression of pro-inflammatory mediators in the rat brain. These results suggested that PCE may be effective in preventing or slowing the development of neurological disorders, including Alzheimer's disease, by improving cognitive and memory function because of its anti-inflammation activity in the brain.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.21 no.6
• /
• pp.1462-1469
• /
• 2007

This study has been carried out to understand the effect of Gangsim-tang on the hyperglycemic mice induced with Streptozotocin(STZ). The 60 mg/kg of streptozotocin(STZ) was treated into mice twice by 24 hrs interval and then 120 mg/kg STZ was treated again 3 days after the earlier treated. Control group was administered mice with 0.9％ saline(2ml/kg), and experimental groups were administered Gangsim-tang extract(GA group, 10 ㎎/㎏/day; GB group, 30 mg/kg/day) after hyperglycemic induction daily for 6 weeks. The body weight of experimental groups was lower than control. The blood glucose concentration increased continuously, reaching to 298.9 mg/dl after 6 weeks, however, experimental groups of the GA and GB groups significantly(p<0.01) decreased in the 4, 5, and 6 weeks groups. Blood glucose tolerance test was not significant between control and experimental groups. We examined the blood transaminase activities to know the effect of herbal medicine on liver function. The glutamic-oxaloacetic transaminase(GOT) activity was lower in group GB than in control. The glutamic-pyruvic transaminse(GPT) activity was lower in group GA and GB than in control. The superoxide dismutase(SOD) and catalase activities were higher in the group GA compared to control. The results of immunohistochemical study, Langerhan's islet of pancreas was destructed by treatment of STZ in the control, and a few of insulin positive cells observed in the control and experimental group. These results suggest that administration of Gangsim-tang extract to the hyperglycemic mice induced with STZ not regeneration of ${\beta}-cells$ but control of the blood glucose level.

• Journal of Power Electronics
• /
• v.15 no.1
• /
• pp.190-201
• /
• 2015

This paper uses the switching function approach to present a simple state model of the Vienna-type rectifier. The approach introduces the relationship between the DC-link neutral point voltage and the AC side phase currents. A novel direct power control (DPC) strategy, which is based on the sliding mode control (SMC) for Vienna I rectifiers, is developed using the proposed power model in the stationary ${\alpha}-{\beta}$ reference frames. The SMC-based DPC methodology directly regulates instantaneous active and reactive powers without transforming to a synchronous rotating coordinate reference frame or a tracking phase angle of grid voltage. Moreover, the required rectifier control voltages are directly calculated by utilizing the non-linear SMC scheme. Theoretically, active and reactive power flows are controlled without ripple or cross coupling. Furthermore, the fixed-switching frequency is obtained by employing the simplified space vector modulation (SVM). SVM solves the complicated designing problem of the AC harmonic filter. The simplified SVM is based on the simplification of the space vector diagram of a three-level converter into that of a two-level converter. The dwelling time calculation and switching sequence selection are easily implemented like those in the conventional two-level rectifier. Replacing the current control loops with power control loops simplifies the system design and enhances the transient performance. The simulation models in MATLAB/Simulink and the digital signal processor-controlled 1.5 kW Vienna-type rectifier are used to verify the fast responses and robustness of the proposed control scheme.

• Journal of Microbiology and Biotechnology
• /
• v.18 no.7
• /
• pp.1278-1285
• /
• 2008

The intestinal epithelial cell (IEC) layer of the intestinal tract makes direct contact with a number of microbiota communities, including bacteria known to have deleterious health effects. IECs possess innate protective strategies against pathogenic challenge, which primarily involve the formation of a physicochemical barrier. Intestinal tract mucins are principal components of the mucus layer on epithelial surfaces, and perform a protective function against microbial damage. However, little is currently known regarding the interactions between probiotics/pathogens and epithelial cell mucins. The principal objective of this study was to determine the effects of Lactobacillus on the upregulation of MUC2 mucin and the subsequent inhibition of E. coli O157:H7 attachment to epithelial cells. In the current study, the attachment of E. coli O157:H7 to HT-29 intestinal epithelial cells was inhibited significantly by L. acidophilus A4 and its cell extracts. It is also important to note that the expression of MUC2 mucin was increased as the result of the addition of L. acidophilus A4 cell extracts (10.0 mg/ml), which also induced a significant reduction in the degree to which E. coli O157:H7 attached to epithelial cells. In addition, the mRNA levels of IL-8, IL-1$\beta$, and TNF-$\alpha$ in HT-29 cells were significantly induced by treatment with L. acidophilus A4 extracts. These results indicate that MUC2 mucin and cytokines are important regulatory factors in the immune systems of the gut, and that selected lactobacilli may be able to induce the upregulation of MUC2 mucin and specific cytokines, thereby inhibiting the attachment of E. coli O157:H7.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.3
• /
• pp.377-384
• /
• 1998

Gold compounds depress phagocytic cell responses, including chemotaxis, and respiratory burst. However, the effects of gold compounds on the function of phagocytic cells are variable according to the preparation of medicine. In this study, effect of tetrachloroauric acid on activated neutrophil responses, including respiratory burst, lysosomal enzyme release and change of intracellular $Ca^{2+}$ level and on the synthesis of interleukin-8 and granulocyte-macrophage colony stimulating factor by macrophages was studied. This study further examines how gold compounds affect the activation processes. The respiratory burst stimulated by complement C5a, degraded IgG and PMA in neutrophils was inhibited by tetrachloroauric acid. In contrast to C5a and degraded IgG, PMA-stimulated superoxide production was weakly inhibited by tetrachloroauric acid. Staurosporine, genistein, EGTA and verapamil inhibited superoxide and $H_2O_2$ production caused by C5a and degraded IgG. PMA-stimulated superoxide production was inhibited by staurosporine but was not affected by genistein. Tetrachloroauric acid, genistein, EGTA and verapamil inhibited the release of acid phosphatase and myeloperoxidase, while the effect of staurosporine was not detected. The synthesis of interleukin-8 and granulocyte-macrophage colony stimulating factor by $interleukin-1{\beta}$ in macrophages was inhibited by tetrachloroauric acid. Preincubation with tetrachloroauric acid, genistein, EGTA and verapamil, the elevation of [$Ca^{2+}_i$] evoked by C5a was inhibited. Store-regulated $Ca^{2+}$ entry in thapsigargin-pretreated neutrophils was decreased by the addition of tetrachloroauric acid and genistein. The effect of staurosporine on intracellular $Ca^{2+}$ mobilization was not observed. In conclusion, tetrachloroauric acid may suppress neutrophil responses through its inhibitory action on elevation of intracellular $Ca^{2+}$ level and protein kinase C. It might exhibit an inhibitory effect on the action of protein tyrosine kinase. Tetrachloroauric acid depresses cytokine production by macrophages.