• Herbal Formula Science
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• v.30 no.1
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• pp.11-18
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• 2022

Objectives: In this study, we aim to demonstrate an effect of crab water extract (CWE) on reflux esophagitis (RE) using lipopolysaccharide (LPS)-induced Raw 264.7 cell and rat model. Methods: To investigate on LPS-induced Raw 264.7 cell, CWE was co-treated with LPS. CWE suppressed Nitric Oxide (NO) production which increased by LPS treatment. Also, CWE showed no cytotoxicity at the concentrations range from 500 ㎍/㎖ to 2000 ㎍/㎖. Next, to investigate the protective effects of CWE on RE rat model, eighteen rats were divided in to three groups: sham group, reflux esophagitis group, and reflux esophagitis pre-treated with 100 mg/kg CWE 1 h before surgery. RE was induced by a pylorus and forestomach ligation operation and all rats were sacrificed after 4 h 30 min from surgery. Results: In gross examination, the CWE administration attenuated esophageal mucosal injury upon histological evaluation of reflux esophagus of rats. The CWE downregulated the expression levels of proteins related to inflammation, such as COX-2 and TNF-α in the esophagus tissue. In addition, the CWE suppressed the NF-κB and IκB-α activation. Conclusions: Based on these findings, we concluded that CWE could possess protective effect against damage to the esophagus due to reflux esophagitis.

• The Journal of Korean Obstetrics and Gynecology
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• v.30 no.2
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• pp.1-15
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• 2017

Objectives: The object of this study was to identify the anti-inflammatory effects of Patrinia scabiosaefolia aqueous extract (PSE). Methods: RAW 264.7 cells were pre-treated with PSE and then incubated with or without lipopolysaccharide (LPS). Cell viability, production of nitric oxide (NO), secretion of pro-inflammatory cytokine, activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-${\kappa}B$) were measured. In addition, we observed mice survival rate after LPS and their cytokine levels of serum. We also observed inflammatory and hemorrhagic change on the histological sections of the liver. Results: PSE inhibited LPS-induced NO production, interleukin (IL)-6 secretion, c-Jun NH2-terminal kinase (JNK) and NF-${\kappa}B$ activation. In addition, PSE reduced the death rate of LPS-induced mice and IL-6 production on the serum of mice. PSE inhibited inflammation and hemorrhage on liver tissue as well. Conclusions: The results suggest that PSE have anti-inflammatory effects by inhibited NF-${\kappa}B$ and JNK activation, IL-6 secretion, and NO production. So PSE may be effective treatment for the inflammatory disease.

• BMB Reports
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• v.39 no.5
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• pp.618-625
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• 2006

The infiltration of both monocyte and activated T cells in the skin is one of critical steps in the development of UVB-induced inflammation. Upregulation of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1) on the surface of keratinocytes plays an important role in this process. In this study, we examined the molecular mechanism responsible for UVB-induced expression of ICAM-1 and subsequent monocyte adhesion by keratinocyte. We observed that (1) UVB induced protein and mRNA expression of ICAM-1 in a dose- and time-dependent manner in human keratinocyte cell HaCaT; (2) UVB induced the translocation of NF-kappaB and inhibition of NF-kappaB by NF-kappaB inhibitors suppressed UVB-induced mRNA and protein expression of ICAM-1; (3) UVB increased the intracellular level of reactive oxygen species (ROS) by HaCaT cells; (4) UVB-induced increase of intracellular ROS level was suppressed by pre-treatment with diphenyl iodonium (DPI) and N-acetyl cysteine (NAC); and (5) inhibition of UVB-induced ROS production by DPI or NAC suppressed UVB-mediated translocation of NF-kappaB, expression of ICAM-1 and subsequent monocyte adhesion in HaCaT cells. These results suggest that UVB-induced ROS is involved in the translocation of NF-kappaB which is responsible for expression of ICAM-1 and subsequent increased monocyte adhesion in human keratinocyte.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.125-134
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• 2015

Acute graft-versus-host-disease (GVHD) is characterized by selective damage to the liver, the skin, and the gastrointestinal tract. Following allogeneic hematopoietic stem cell transplantation, donor bone marrow (BM) cells repopulate the immune system of the recipient. We previously demonstrated that the acute intestinal GVHD (iGVHD) mortality rate was higher in MyD88-deficient BM recipients than that in the control BM recipients. In the present study, the role of MyD88 (expressed by donor BM) in the pathophysiology of hepatic GVHD (hGVHD) was examined. Unlike iGVHD, transplantation with MyD88-deficient T-cell depleted (TCD) BM attenuated hGVHD severity and was associated with low infiltration of T cells into the liver of the recipients. Moreover, GVHD hosts, transplanted with MyD88-deficient TCD BM, exhibited markedly reduced expansion of $CD11b^+Gr-1^+$ myeloidderived suppressor cells (MDSC) in the liver. Adoptive injection of the MDSC from wild type mice, but not MyD88-deficient mice, enhanced hepatic T cell infiltration in the MyD88-deficient TCD BM recipients. Pre-treatment of BM donors with LPS increased MDSC levels in the liver of allogeneic wild type BM recipients. In conclusion, hGVHD and iGVHD may occur through various mechanisms based on the presence of MyD88 in the non-T cell compartment of the allograft.

• Journal of Dental Anesthesia and Pain Medicine
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• v.18 no.6
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• pp.349-359
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• 2018

Background: Propofol is an intravenous anesthetic which has antioxidant effects due to its similarity in molecular structure to ${\alpha}$-tocopherol. It has been reported that ${\alpha}$-tocopherol increases osteoclast fusion and bone resorption. Here, we investigated the effects of propofol on signaling pathways of osteoclastogenic gene expression, as well as osteoclastogenesis and bone resorption using bone marrow-derived macrophages (BMMs). Methods: BMMs were cultured with macrophage colony-stimulating factor (M-CSF) alone or M-CSF plus receptor activator of nuclear factor kappa B ligand (RANKL) in the presence of propofol ($0-50{\mu}M$) for 4 days. Mature osteoclasts were stained for tartrate-resistant acid phosphatase (TRAP) and the numbers of TRAP-positive multinucleated osteoclasts were counted. To examine the resorption activities of osteoclasts, a bone resorption assay was performed. To identify the mechanism of action of propofol on the formation of multinucleated osteoclasts, we focused on dendritic cell-specific transmembrane protein (DC-STAMP), a protein essential for pre-osteoclastic cell fusion. Results: Propofol increased the formation of TRAP-positive multinucleated osteoclasts. In addition, the bone resorption assay revealed that propofol increased the bone resorption area on dentin discs. The mRNA expression of DC-STAMP was upregulated most strongly in the presence of both RANKL and propofol. However, SB203580, a p38 inhibitor, significantly suppressed the propofol/RANKL-induced increase in mRNA expression of DC-STAMP. Conclusion: We have demonstrated that propofol enhances osteoclast differentiation and maturation, and subsequently increases bone resorption. Additionally, we identified the regulatory pathway underlying osteoclast cell-cell fusion, which was enhanced by propofol through p38-mediated DC-STAMP expression.

• Korean Journal of Food Science and Technology
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• v.39 no.2
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• pp.181-188
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• 2007

This study examined the effects of green tea extract supplementation (500 or 1,000 mg/kg b.w. per day) in conjunction with an atherogenic diet (10% coconut oil (w/w), 0.1% cholesterol) on plasma lipid composition, regression of pre-existing foam cells, and on the mRNA levels of hepatic HMG-CoA reductase and LDL receptor. Compared to groups fed only with the atherogenic diet, the addition of green tea extract to atherogenic diet-fed groups significantly down-regulated plasma triglyceride and total cholesterol levels, dose-dependently. Supplementation of 1,000 mg/kg b.w. of green tea extract with the atherogenic diet induced significant up-regulation of both HMG-CoA reductase and LDL receptor messenger RNA levels in liver as compared to the group receiving green tea extract supplementation at 500 mg/kg b.w. The F1B hamsters fed the atherogenic diet had greater foam cell accumulation compared to those fed a normal diet, or the atherogenic diet supplemented with green tea extract. Regression of fatty streak lesions was achieved by atherosclerosis in fat- and cholesterol-fed hamsters and this effect was associated with down-regulation of plasma cholesterol and up-regulation of hepatic LDL receptor expression.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1177-1182
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• 2012

Protein kinase C (PKC) has been implicated in carcinogenesis and displays variable expression profiles during cancer progression. Studies of dietary phytochemicals on cancer signalling pathway regulation have been conducted to search for potent signalling regulatory agents. The present study was designed to evaluate any suppressive effect of maslinic acid on PKC expression in human B-lymphoblastoid cells (Raji cells), and to identify the PKC isoforms expressed. Effects of maslinic acid on PKC activity were determined using a PepTag$^{(R)}$ assay for non-radioactive detection of PKC. The highest expression in Raji cells was obtained at 20 nM PMA induced for 6 hours. Suppressive effects of maslinic acid were compared with those of four PKC inhibitors (H-7, rottlerin, sphingosine, staurosporine) and two triterpenes (oleanolic acid and ursolic acid). The $IC_{50}$ values achieved for maslinic acid, staurosporine, H-7, sphingosine, rottlerin, ursolic acid and oleanolic acid were 11.52, 0.011, 0.767, 2.45, 5.46, 27.93 and $39.29\;{\mu}M$, respectively. Four PKC isoforms, PKC ${\beta}I$, ${\beta}II$, ${\delta}$, and ${\zeta}$, were identified in Raji cells via western blotting. Maslinic acid suppressed the expression of PKC ${\beta}I$, ${\delta}$, and ${\zeta}$ in a concentration-dependent manner. These preliminary results suggest promising suppressive effects of maslinic acid on PKC activity in Raji cells. Maslinic acid could be a potent cancer chemopreventive agent that may be involved in regulating many downstream signalling pathways that are activated through PKC receptors.

• YAKHAK HOEJI
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• v.43 no.2
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• pp.278-284
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• 1999

This study deals with the biological changes in mice after ${\gamma}-irradiated$. Four weeks old BALA/c mice were irradiated with 6.5Gy of ${\gamma}-ray$ on the fifth day after oral administration of radioprotectants such as ascorbic acid, tocopherol and cysteine. Control group was irradiated with 6.5Gy without pre-administration of radioprotectors. Blood cells and sperm cells were counted and body, testis and spleen were weighed 3 days after irradiation. And also liver antioxidant activity and range of spleen immune cells were measured. Differences in most biological parameters were not clearly distinguished between experimental groups. However, the relative spleen weight, the relative testis weight and the population size of spleen immune cells such as T helper cells, B cells and macrophages measured by means of FACS showed significant difference between irradiated and radioprotectant administered group. It is concluded that the relative spleen weight, the relative testis weight and the population size of spleen immune cells are easy and useful parameters for assessing the effect of radioprotective substances and for quantifying biological damage of radiation, as well.

• Smart Media Journal
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• v.11 no.5
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• pp.26-37
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• 2022

In this paper, images are automatically acquired to control the initial disease of strawberries among facility cultivation crops, and disease analysis is performed using the EfficientNet model to inform farmers of disease status, and disease diagnosis service is proposed by experts. It is possible to obtain an image of the strawberry growth stage and quickly receive expert feedback after transmitting the disease diagnosis analysis results to farmers applications using the learned EfficientNet model. As a data set, farmers who are actually operating facility cultivation were recruited and images were acquired using the system, and the problem of lack of data was solved by using the draft image taken with a cell phone. Experimental results show that the accuracy of EfficientNet B0 to B7 is similar, so we adopt B0 with the fastest inference speed. For performance improvement, Fine-tuning was performed using a pre-trained model with ImageNet, and rapid performance improvement was confirmed from 100 Epoch. The proposed service is expected to increase production by quickly detecting initial diseases.

• Journal of Animal Reproduction and Biotechnology
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• v.37 no.4
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• pp.292-297
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• 2022

Direct injection of CRISPR/Cas9 into zygotes enables the production of genetically modified nonhuman primates (NHPs) essential for modeling specific human diseases, such as Usher syndrome, and for developing novel therapeutic strategies. Usher syndrome is a rare genetic disease that causes loss of hearing, retinal degeneration, and problems with balance, and is attributed to a mutation in MYO7A, a gene that encodes an uncommon myosin motor protein expressed in the inner ear and retinal photoreceptors. To produce an Usher syndrome type 1B (USH1B) rhesus macaque model, we disrupted the MYO7A gene in developing zygotes. Identification of appropriately edited MYO7A embryos for knockout embryo transfer requires sequence analysis of material recovered from a trophectoderm (TE) cell biopsy. However, the TE biopsy procedure is labor intensive and could adversely impact embryo development. Recent studies have reported using cell-free DNA (cfDNA) from embryo culture media to detect aneuploid embryos in human in vitro fertilization (IVF) clinics. The cfDNA is released from the embryo during cell division or cell death, suggesting that cfDNA may be a viable resource for sequence analysis. Moreover, cfDNA collection is not invasive to the embryo and does not require special tools or expertise. We hypothesized that selection of appropriate edited embryos could be performed by analyzing cfDNA for MYO7A editing in embryo culture medium, and that this method would be advantageous for the subsequent generation of genetically modified NHPs. The purpose of this experiment is to determine whether cfDNA can be used to identify the target gene mutation of CRISPR/Cas9 injected embryos. In this study, we were able to obtain and utilize cfDNA to confirm the mutagenesis of MYO7A, but the method will require further optimization to obtain better accuracy before it can replace the TE biopsy approach.