• Journal of Ginseng Research
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• v.47 no.4
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• pp.524-533
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• 2023

Background: Obesity is a risk factor for aging and many diseases, and the disorder of lipid metabolism makes it prominent. This study aims to investigate the effect of ginsenoside Rg1 on aging, lipid metabolism and stress resistance Methods: Rg1 was administered to Caenorhabditis elegans (C. elegans) cultured in NGM or GNGM. The lifespan, locomotory activity, lipid accumulation, cold and heat stress resistance and related mRNA expression of the worms were examined. Gene knockout mutants were used to clarify the effect on lipid metabolism of Rg1. GFP-binding mutants were used to observe the changes in protein expression Results: We reported that Rg1 reduced lipid accumulation and improved stress resistance in C. elegans. Rg1 significantly reduced the expression of fatty acid synthesis-related genes and lipid metabolism-related genes in C. elegans. However, Rg1 did not affect the fat storage in fat-5/fat-6 double mutant or nhr-49 mutant. Combined with network pharmacology, we clarified the possible pathways and targets of Rg1 in lipid metabolism. In addition, Rg1-treated C. elegans showed a higher expression of anti-oxidative genes and heat shock proteins, which might contribute to stress resistance Conclusion: Rg1 reduced fat accumulation by regulating lipid metabolism via nhr-49 and enhanced stress resistance by its antioxidant effect in C. elegans.

• Journal of Ginseng Research
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• v.41 no.2
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• pp.134-143
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• 2017

Background: The prevalence of allergic inflammatory diseases such as atopic dermatitis (AD), asthma, and allergic rhinitis worldwide has increased and complete recovery is difficult. Korean Red Ginseng, which is the heat-processed root of Panax ginseng Meyer, is widely and frequently used as a traditional medicine in East Asia. In this study, we investigated whether Korean Red Ginseng water extract (RGE) regulates the expression of proinflammatory cytokines and chemokines via the mitogen-activated protein kinases (MAPKs)/nuclear factor kappa B ($NF-{\kappa}B$) pathway in allergic inflammation. Methods: Compound 48/80-induced anaphylactic shock and 1-fluoro-2,4-dinitrobenzene (DNFB)-induced AD-like skin lesion mice models were used to investigate the antiallergic effects of RGE. Human keratinocytes (HaCaT cells) and human mast cells (HMC-1) were also used to clarify the effects of RGE on the expression of proinflammatory cytokines and chemokines. Results: Anaphylactic shock and DNFB-induced AD-like skin lesions were attenuated by RGE administration through reduction of serum immunoglobulin E (IgE) and interleukin (IL)-6 levels in mouse models. RGE also reduced the production of proinflammatory cytokines including $IL-1{\beta}$, IL-6, and IL-8, and expression of chemokines such as IL-8, thymus and activation-regulated chemokine (TARC), and macrophage-derived chemokine (MDC) in HaCaT cells. Additionally, RGE decreased the release of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), $IL-1{\beta}$, IL-6, and IL-8 as well as expressions of chemokines including macro-phage inflammatory protein $(MIP)-1{\alpha}$, $MIP-1{\beta}$, regulated on activation, normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein (MCP)-1, and IL-8 in HMC-1 cells. Furthermore, our data demonstrated that these inhibitory effects occurred through blockage of the MAPK and $NF-{\kappa}B$ pathway. Conclusion: RGE may be a useful therapeutic agent for the treatment of allergic inflammatory diseases such as AD-like dermatitis.

• International Journal of Industrial Entomology and Biomaterials
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• v.1 no.2
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• pp.171-175
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• 2000

Determined sequences of 384 randomly selected clones in a PCR-based cDNA library of Antheraea yamamai could identify expressed sequence tags (ESTs) of highly expressed gene. One EST (fibroin) appeared 15 times, one EST (40S ribosomal protein S18) twelve times, one EST (ribosomal protein S24a) eleven times, ten times (ribosomal protein S8), nine times (60S ribosomal protein L10A), seven times (60S ribosomal protein S15A, S17, S17 and seroin), six times (ribosomal protein S8), five times (ribosomal protein S24, mariner transposase and P8 protein), four times (serpin 2), three times (heat shock protein 70 and poly A binding protein), and the remaining 6 ESTs twice (amylase, KIAA1006, elongation factor-1, transposon mag, translation initiation factor 4C, QM protein, transposase). Therefore, the 94 EST make it possible to identify 24 redundant clones that are candidates for highly expressed genes in posterior silk gland of this insect. The 24 redundant EST clones were identified in GenBank, but none of them was related to A. yamamai, suggesting that there are many unidentified genes which are highly expressed in the A. yamamai genome.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.241-246
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• 2003

Bambusae Caulis in Liquamen(BCL) has been used to relieve the cough and asthma, and remove the phlegm in traditional Oriental medicine. In recent years, it was studied for its antiinflammatory, antiallergenic, immune-modulating, and anticarcinogenic capabilities. This experiment was performed to evaluate the microarray profiles of CD genes in human mast cells before and after BCL treatment. The results are as follows: The expression of 51 of the genes studied was up-regulated in the Bel-treated group; they include the genes coding L apoferritin, beta-2-microglobulin, ferritin light polypeptide, CD63, monocyte chemotactic and activating fact, heme oxygenase 1, CD140a, integrin alpha M, colony stimulating factor 2 receptor, eukaryotic translation elongation factor, CD37, interleukin 18, NADH dehydrogenase 1 beta, CD48, 5-lipoxygenase activating protein, interleukin 4, ribosomal protein L5, GABA(A) receptor-associated protein, beta-tubulin, integrin beta 1, CD162, CD32, lymphotoxin beta, alpha-tublin, integrin alpha L, CD2, CD151, CD331, 90 kDa heat shock protein, CD59, CD3Z, microsomal glutathione S-transferase 2, CD33, CD162R, cyclophilinA, CD84, interleukin 9 receptor, interleukin 11, CD117, CD39-Like 2, and so forth. The expression of 7 of the genes studied was down-regulated in the BCL-treated group; they include the genes coding con, CD238, SCF, CD160, CD231, CD24, and CD130. Consequently, the treatment of BCL on the human mast cells increased the expression of 51 genes and decreased the expression of 7 genes. These data would provide a fundamental basis to the traditional applications of Bambusae Caulis in Liquamen.

• Korean Journal of Environmental Agriculture
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• v.38 no.4
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• pp.296-306
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• 2019

BACKGROUND: Temperature is known to be the main factor affecting development, growth and reproduction of organisms and also a physical factor directly related to insect survival. Insects as ectothermal species should be responsive to climate changes for their survival and develop various survival strategies under the unfavorable temperature such as low temperature. The purpose of this study is to identify genes contributing to adaptation of low temperature. METHODS AND RESULTS: To identify genes contributing to adaptation of low temperature, the transcriptomic data were obtained from fat body in Plutella xyostella larvae via next generation sequencing. We identified structural proteins, heat shock proteins, antioxidant enzymes, detoxification proteins, and cryoprotectant mobilization and biosynthesis-related proteins. Genes encoding chitinase, cuticular protein, Hsp23, chytochrome protein, Glutathione S transferase, and phospholipase 2 were up-regulated under low temperature. Proteins related to energy metabolism such as UDP-glycosy ltransferase, trehalase and trehalose transporter were down-regulated. CONCLUSION: When insect pests were exposed to low temperature, changes in gene expression of fat body could provide some hints for understanding temperature adaptation strategies.

• Interdisciplinary Bio Central
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• v.5 no.4
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• pp.9.1-9.7
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• 2013

Introduction: Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein (HSP), which belongs to HSP90 family. It plays important roles in regulating mitochondrial integrity, protecting against oxidative stress, and inhibiting cell death. Recent studies suggest that TRAP1 is linked to mitochondria and its metabolism. In this study, we established TRAP1 transgenic mice and performed partial hepatectomy (PH) on wild-type (WT) and TRAP1 transgenic mice to investigate the function of TRAP1 during liver regeneration. Results and Discussion: We found that TRAP1 was highly expressed in liver as well as kidney. In addition, liver regeneration slightly decreased together with increased fatty liver and inflammation at 72 hr after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. These results suggest that TRAP1 plays a critical role in liver energy balance by regulating lipid accumulation during liver regeneration. Conclusions and Prospects: To our knowledge, we reported, for the first time, that liver regeneration slightly reduced together with increased fat accumulations after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. Overexpression of TRAP1 might affect liver regeneration via disturbing mitochondrial function leading to fatty liver in vivo.

• Journal of Chest Surgery
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• v.50 no.3
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• pp.153-162
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• 2017

Background: The mesenchymal-epithelial transition factor (MET) receptor can be overexpressed in solid tumors, including small cell lung cancer (SCLC). However, the molecular mechanism regulating MET stability and turnover in SCLC remains undefined. One potential mechanism of MET regulation involves the C-terminus of Hsp70-interacting protein (CHIP), which targets heat shock protein 90-interacting proteins for ubiquitination and proteasomal degradation. In the present study, we investigated the functional effects of CHIP expression on MET regulation and the control of SCLC cell apoptosis and invasion. Methods: To evaluate the expression of CHIP and c-Met, which is a protein that in humans is encoded by the MET gene (the MET proto-oncogene), we examined the expression pattern of c-Met and CHIP in SCLC cell lines by western blotting. To investigate whether CHIP overexpression reduced cell proliferation and invasive activity in SCLC cell lines, we transfected cells with CHIP and performed a cell viability assay and cellular apoptosis assays. Results: We found an inverse relationship between the expression of CHIP and MET in SCLC cell lines (n=5). CHIP destabilized the endogenous MET receptor in SCLC cell lines, indicating an essential role for CHIP in the regulation of MET degradation. In addition, CHIP inhibited MET-dependent pathways, and invasion, cell growth, and apoptosis were reduced by CHIP overexpression in SCLC cell lines. Conclusion: C HIP is capable of regulating SCLC cell apoptosis and invasion by inhibiting MET-mediated cytoskeletal and cell survival pathways in NCI-H69 cells. CHIP suppresses MET-dependent signaling, and regulates MET-mediated SCLC motility.

• Biomolecules & Therapeutics
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• v.22 no.4
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• pp.295-300
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• 2014

The actin cytoskeleton plays an important role in macrophage-mediated inflammatory responses by modulating the activation of Src and subsequently inducing nuclear factor (NF)-${\kappa}B$ translocation. In spite of its critical functions, few papers have examined how the actin cytoskeleton can be regulated by the activation of toll-like receptor (TLR). Therefore, in this study, we further characterized the biological value of the actin cytoskeleton in the functional activation of macrophages using an actin cytoskeleton disruptor, cytochalasin B (Cyto B), and explored the actin cytoskeleton's involvement in morphological changes, cellular attachment, and signaling events. Cyto B strongly suppressed the TLR4-mediated mRNA expression of inflammatory genes such as cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-${\alpha}$, and inducible nitric oxide (iNOS), without altering cell viability. This compound also strongly suppressed the morphological changes induced by lipopolysaccharide (LPS), a TLR4 ligand. Cyto B also remarkably suppressed NO production under non-adherent conditions but not in an adherent environment. Cyto B did not block the co-localization between surface glycoprotein myeloid differentiation protein-2 (MD2), a LPS signaling glycoprotein, and the actin cytoskeleton under LPS conditions. Interestingly, Cyto B and PP2, a Src inhibitor, enhanced the phagocytic uptake of fluorescein isothiocyanate (FITC)-dextran. Finally, it was found that Cyto B blocked the phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at 1 min and the phosphorylation of heat shock protein 27 (HSP27) at 5 min. Therefore, our data suggest that the actin cytoskeleton may be one of the key components involved in the control of TLR4-mediated inflammatory responses in macrophages.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.7
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• pp.3471-3476
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• 2012

Background and Objective: Histone deacetylase (HDAC) inhibitors represent a promising class of potential anticancer agents for treatment of human malignancies. In this study, we investigated the effect of trichostatin A (TSA), one such HDAC inhibitor, in combination with docetaxel (TXT), a cytotoxic chemotherapy agent or erlotinib, a novel molecular target therapy drug, on lung cancer A549 cells. Methods: A549 cells were treated with TXT, erlotinib alone or in combination with TSA, respectively. Cell viability, apoptosis, and cell cycle distribution were evaluated using MTT (3- (4, 5-dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide) assay, Hochst33258 staining and flow cytometry. Moreover, immunofluorescent staining and Western blot analysis were employed to examine alterations of ${\alpha}$-tubulin, heat shock protein 90 (hsp90), epidermal growth factor receptor (EGFR), and caspase-3 in response to the different exogenous stimuli. Results: Compared with single-agent treatment, co-treatment of A549 cells with TSA/TXT or TSA/erlotinib synergistically inhibited cell proliferation, induced apoptosis, and caused cell cycle delay at the $G_2/M$ transition. Treatment with TSA/TXT or TSA/erlotinib led to a significant increase of cleaved caspase-3 expression, also resulting in elevated acetylation of ${\alpha}$-tubulin or hsp90 and decreased expression of EGFR, which was negatively associated with the level of acetylated hsp90. Conclusions: Synergistic anti-tumor effects are observed between TXT or erlotinib and TSA on lung cancer cells. Such combinations may provide a more effective strategy for treating human lung cancer.

• The Journal of the Korean Society for Microbiology
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• v.35 no.4
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• pp.299-308
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• 2000

Recently developed cDNA microarray or DNA chip technology allows expression monitoring of expression of hundreds and thousands of genes simultaneously and provides a format for identifying genes as well as changes in their activity. In order to search for changes in gene expression after X irradiation in HL60 cells, cDNA microarray technique was done. In this study, expression of 588 human genes (including oncogenes, tumor suppressor genes, cell cycle regulator genes, intracellular signal transduction modulator genes, apoptosis related genes, transcription factor genes, growth factors and receptor genes, cytokine genes, etc) were analyzed. For cDNA microarray analysis mRNAs were extracted from control and 8 Gy-irradiated HL60 cells. As a result the changes in expression of several genes were observed. This alteration of gene expression was confirmed by reverse transcription-polymerase chain reaction. The expression of heat shock 60 KD protein, c-jun, erythroid differentiation factor, CPP32, myeloid cell nuclear differentiation antigen, MAP kinase-activated protein kinase, interleukin-8, monocyte chemotactic peptide 1 and RANTES genes was increased, but the expression of p55CDC gene was decreased after X irradiation.