• Korean Journal of Veterinary Research
• /
• v.34 no.2
• /
• pp.275-286
• /
• 1994

Plasma protein which has been known as one of nonspecific immunostimulators was added to feedstuff to examine its effect on the enhancement of cellular immune response in porcine immune system. A total of 40 piglets, 20 male and 20 female each, were fed for 30 days with or without plasma protein. The peripheral blood were collected and analyzed for the investigation of leukocyte subpopulations and their activities by using a panel of monoclonal antibodies specific to porcine leukocyte differentiation antigens and flow cytometry. The results obtained as follows. 1. Total weight gain, daily feed intake and feed conversion rate for 10 days were significantly improved to 56%, 20% and 22% in the piglets fed plasma protein, respectively. 2. A significant increase in N (null or non T/non B) cells was also noticed. Leukocyte proportion from piglets fed plasma protein was 20.2-24.7%, otherwise that from piglets fed without plasma protein was 12.3-13.4%, respectively. 3. A significant increase in the proportion of B cells and cells expressing poCD1 was not found in piglets fed plasma protein. 4. Reaction with monoclonal antibodies specific to adhesion molecules, poCD11a, poCD11b, poCD44 and poCD45A and poCD45B, has shown that leukocyte subpopulation from piglets fed plasma protein did not significantly higher than that from piglets fed without plasma protein. 5. Total proportion of granulocytes and monocytes was about 50% in both group and the proportion after treated with Hypaque/Ficoll was 2.7% and 5.8% in each group, respectively.

• BMB Reports
• /
• v.46 no.8
• /
• pp.410-415
• /
• 2013

Adhesion molecules such as ICAM-1 are important in the infiltration of leukocytes into the site of inflammation. In this study, we investigated the inhibitory effects of curcumin on ICAM-1 expression and monocyte adhesiveness as well as its underlying action mechanism in the TNF-${\alpha}$-stimulated keratinocytes. Curcumin induced expression of heme oxygenase-1 (HO-1) in the human keratinocyte cell line HaCaT. In addition, curcumin induced Nrf2 activation in dose- and time-dependent manners in the HaCaT cells. Curcumin suppressed TNF-${\alpha}$-induced ICAM-1 expression and subsequent monocyte adhesion, which were reversed by the addition of tin protoporphyrin IX (SnPP), a specific inhibitor of HO-1, or HO-1 knockdown using siRNA. Furthermore, Nrf2 knockdown using siRNA reversed the inhibitory effect of curcumin on the TNF-${\alpha}$-induced ICAM-1 expression and adhesion of monocytes to keratinocytes. These results suggest that curcumin may exert its anti-inflammatory activity by suppressing the TNF-${\alpha}$-induced ICAM-1 expression and subsequent monocyte adhesion via expression of HO-1 in the keratinocytes.

• The Korea Journal of Herbology
• /
• v.23 no.1
• /
• pp.29-38
• /
• 2008

Objectives : Evodia officinalis DODE (EO), an herbal plant, has been widely used in traditional Korean medicine for the treatment of vascular diseases such as hypertension. The crude extract of EO contains phenolic compounds that are effective in protecting liver microsomes, hepatocytes, and erythrocytes against oxidative damage. But EO has been little found to have an anti-inflammatory activity. We investigated anti-inflammatory activity of EO in RAW 264.7 cells and human umbilical vein endothelial cells (HUVECs). Methods : Cytotoxic activity of EO on RAW 264.7 cells was investigated by using 5-(3-caroboxymeth-oxyphenyl)-2H-tetra-zolium inner salt (MTS) assay. The nitric oxide (NO) production was measured by Griess reagent system. And proinflammatory cytokines were measured by ELISA kit. The levels of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression were measured by flow cytometer. Results : EO decreased LPS-induced NO production in RAW 264.7 cells. The inhibitory activity of EO on LPS-induced NO release is probably associated with suppressing TNF-${\alpha}$, IL-6 and MCP-1 formation. These results indicate that EO has potential as an anti-inflammatory agent. Moreover, EO decreased TNF-${\alpha}$-induced IL-8, IL-6 production, and ICAM-1 and VCAM-1 expression in HUVECs. Conclusions : EO inhibits TNF-${\alpha}$-induced inflammation via decreasing cytokines production and adhesion molecules expression. These results indicate that EO has potential as an anti-inflammation and anti-artherosclerosis agent.

• Molecules and Cells
• /
• v.40 no.5
• /
• pp.363-370
• /
• 2017

Extrahepatic cholangiocarcinoma (ECC), a malignant tumor of biliary origin, has a poor prognosis with limited treatment options. The KRAS oncogene is the most commonly mutated gene in ECC and one of the factors that predicts a poor prognosis and low survival rate. L1 cell adhesion molecule (L1CAM) is expressed in ECC cells and acts as an independent poor prognostic factor in predicting patient survival. In this study we investigate the functional significance of L1CAM in ECC cells with activating KRAS mutation. We selected an ECC cell line, EGI-1, with activating KRAS mutation, and then confirmed its expression of L1CAM by RT-PCR, western blot analysis, and flow cytometry. The suppression of L1CAM expression (using a specific lentivirus-delivered shRNA) significantly decreased the migratory and invasive properties of EGI-1 cells, without altering their proliferation or survival. Analyses of signaling effectors in L1CAM-depleted and control EGI-1 cells indicated that L1CAM suppression decreased the levels of both phosphorylated MKK4 and total MKK4, together with c-Jun N-terminal kinase (JNK) phosphorylation. Further, exposure to a JNK inhibitor (SP600125) decreased migration and invasion of EGI-1 cells. These results suggest that L1CAM promotes cellular migration and invasion via the induction of MKK4 expression, leading to JNK activation. Our study is the first to demonstrate a functional role for L1CAM in ECC carrying the activating KRAS mutation. Given that KRAS is the most commonly mutated oncogene in ECC, L1CAM may serve as an attractive therapeutic target for ECC cells with activating KRAS mutation.

• Tuberculosis and Respiratory Diseases
• /
• v.43 no.2
• /
• pp.210-220
• /
• 1996

Background : Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. In the process of surface adherence, adhesion molecules have a clear role in intracellular signal pathway of cellular activation. Human alveolar macrophages(HAM) are frequently purified by the adherence procedure after bronchoalveolar lavage. But the experimental data of many reports about alveolar macrophages have ignored the possibility of adhesion-induced cellular activation. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be normal by chest CT. With the measurement of hydrogen peroxide release from adherent HAM to plastic surface and non-adherent HAM with or without additional stimulation of phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), we observed the effect of the adherence to plastic surface. We also evaluated the effect of various biological surfaces on adhesion-induced activation of HAM. Then, to define the intracellular pathway of signal transduction, pretreatment with cycloheximide, pertussis toxin and anti-CD11/CD18 monoclonal antibody was done and we measured hydrogen peroxide in the culture supernatant of HAM. Results : 1) The adherence itself to plastic surface directly stimulated hydrogen peroxide release from human alveolar macrophages and chemical stimuli such as phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine(fMLP) colud not increase hydrogen peroxide release in these adherent macrophages which is already activated. 2) PMA activated human alveolar macrophages irrespective of the state of adhesion. However, fMLP stimulated the release of hydrogen peroxide from the adherent macrophages, but not from the non-adherent macrophages. 3) HAM adherent to A549 cell(type II alveolar epithelium-like human cell line) monolayer released more hydrogen peroxide in response to both PMA and fMLP. This adherence-dependent effect of fMLP was blocked by pretreatment of macrophages with cycloheximide, pertussis toxin and anti-CD18 monoclonal antibody, Conclusion : These results suggest that the stimulatory effect of PMA and fMLP can not be found in adherent macrophage because of the activation of human alveolar macrophage by the adherence to plastic surface and the cells adhered to biologic surface such as alveolar epithelial cells are appropriately responsive to these stimuli. It is also likely that the effect of fMLP on the adherent macrophage requires new protein synthesis via G protein pathway and is dependent on the adhesion between alveolar macrophages and alveolar epithelial cells by virtue of CD11/CD18 adhesion molecules.

• BMB Reports
• /
• v.46 no.11
• /
• pp.544-549
• /
• 2013

High mobility group box 1 (HMGB1) is involved in the pathogenesis of vascular diseases. Unlike activated protein C (APC), the activation of PAR-1 by thrombin is known to elicit proinflammatory responses. To determine whether the occupancy of EPCR by the Gla-domain of APC is responsible for the PAR-1-dependent antiinflammatory activity of the protease, we pretreated HUVECs with the PC zymogen and then activated PAR-1 with thrombin. It was found that thrombin downregulates the HMGB1-mediated induction of both TNF-${\alpha}$ and IL-6 and inhibits the activation of both p38 MAPK and NF-${\kappa}B$ in HUVECs pretreated with PC. Furthermore, thrombin inhibited HMGB1-mediated hyperpermeability and leukocyte adhesion/migration by inhibiting the expression of cell adhesion molecules in HUVECs if EPCR was occupied. Collectively, these results suggest the concept that thrombin can initiate proinflammatory responses in vascular endothelial cells through the activation of PAR-1 may not hold true for normal vessels expressing EPCR under in vivo conditions.

• Korean Journal of Plant Resources
• /
• v.22 no.6
• /
• pp.552-557
• /
• 2009

Allicin, a garlic componente, is believed to provide protection against various diseases including inflammation. Since interactions of the cell adhesion molecules are known to play important roles in mediating inflammation, inhibiting adhesion protein upregulation is a possible therapeutic target. In this study, we demonstrate that TNF-${\alpha}$- and catalase-induced expression of ICAM-1 on human lung epithelial cells (A549) in a dose-dependent manner and catalase expression and activity were also increased in TNF-${\alpha}$-treated cells. Treatment of the TNF-${\alpha}$-treated cells with catalase inhibitor 3-amino-1,2,4-triazole resulted in a significant decreased the level of ICAM-1. These data suggest that induction of ICAM-1 expression by TNF-${\alpha}$ is associated with catalase. In addition, allicin was found to inhibit the TNF-${\alpha}$ induced expression of ICAM-1 on the A549 cells. This compound also inhibited the production of catalase induced by TNF-${\alpha}$, which suggests that the inhibition of ICAM-1 expression by allicin may be due to the modulated production of catalase.

• Journal of Animal Reproduction and Biotechnology
• /
• v.35 no.1
• /
• pp.12-20
• /
• 2020

Cell adhesion plays an important role in the differentiation of the morphogenesis and the trophectoderm epithelium of the blastocyst. In the porcine embryo, CDH1 mediated adhesion initiates at compaction before blastocyst formation, regulated post-translationally via protein kinase C and other signaling molecules. Here we focus on muscle RAS oncogene homolog (M-RAS), which is the closest relative to the RAS related proteins and shares most regulatory and effector interactions. To characterize the effects of M-RAS on embryo compaction, we used gain- and loss-of-function strategies in porcine embryos, in which M-RAS gene structure and protein sequence are conserved. We showed that knockdown of M-RAS in zygotes reduced embryo development abilities and CDH1 expression. Moreover, the phosphorylation of ERK was also decreased in M-RAS KD embryos. Overexpression of M-RAS allows M-RAS KD embryos to rescue the embryo compaction and blastocyst formation. Collectively, these results highlight novel conserved and multiple effects of M-RAS during porcine embryo development.

• Natural Product Sciences
• /
• v.26 no.4
• /
• pp.295-302
• /
• 2020

Cudrania tricuspidata (C. tricuspidata) is a deciduous tree found in Japan, China and Korea. The root, stems, bark and fruit of C. tricuspidata has been used as traditional herbal remedies such as eczema, mumps, acute arthritis and tuberculosis. In this study, we investigated the potential efficacies of this natural compound by focusing on the inhibitory effect of cudraxanthone L (CXL) isolated from the roots of C. tricuspidata on human platelet aggregation. Our study focused on the action of CXL on collagen-stimulated human platelet aggregation, inhibition of platelet signaling molecules such as fibrinogen binding, intracellular calcium mobilization, fibronectin adhesion, dense granule secretion, and thromboxane A2 secretion. In addition, we investigated the inhibitory effect of CXL on thrombin-induced clot retraction. Our results showed that CXL inhibited collagen-induced human platelet aggregation, intracellular calcium mobilization, fibrinogen binding, fibronectin adhesion and clot retraction without cytotoxicity. Therefore, we confirmed that CXL has inhibitory effects on human platelet activities and has potential value as a natural substance for preventing thrombosis.

• Asian Pacific Journal of Cancer Prevention
• /
• v.17 no.4
• /
• pp.1643-1647
• /
• 2016

Since their discovery in 1940, it has been well established that gangliosides are associated with a number of biological pathways and cellular processes such as growth, differentiation and toxin uptake. Gangliosides are glycosphingolipids containing neuraminic acid which are expressed on the plasma membrane of cells particularly in the nervous system. Heterogeneity and structural variation in the carbohydrate chains of gangliosides contributes to unique features of each of these molecules. Thirty five years ago it was discovered that aberrant glycosylation occurs in a variety of human cancers, including aberrant glycosylation of gangliosides. Ganglioside expression in terms of quality and quantity varies in different cancers and different roles may be played. Gangliosides, by affecting the immune system, including esxpression of cytokines and adhesion molecules, may inhibit anti-tumor mechanisms, as well as having direct impact on angiogenesis, cell movement and metastasis. It should be noted that different kinds of gangliosides do not all act by the same mechanisms.