• Korean Journal of Ichthyology
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• v.23 no.1
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• pp.10-20
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• 2011

Genetic determinant for metallothionein (MT), a cysteine-rich protein playing essential roles in metal detoxification and homeostasis, was characterized in the Korean bitterling (Acheilognathus signifer, Cyprinidae), an endemic fish species. The full-length A. signifer MT (AsMT) cDNA (551 bp) is composed of a single open-reading frame (ORF) to encode a polypeptide of 60 amino acids containing 20 cysteine residues whose positions are conserved in most cypriniform MTs. At the genomic level, the AsMT (2,593 bp spanning the 5'-flanking region to the 3'-untranslated region) represented a conserved tripartite (three exons interrupted by two introns) structure with AT-rich introns. The upstream regulatory region (-1,914 bp from the ATG initiation codon) of AsMT displayed various sites and motifs for transcription factors involved in the metal-mediated regulation and stress/immune responses. The AsMT transcript was ubiquitously detected in various organs with variable expression levels, where the ovary and intestine showed the highest expression, while the heart and skeletal muscle represented the lowest level. During an exposure to copper (immersion in $0.5\;{\mu}M$ Cu for 48 h), the levels of AsMT transcripts were significantly elevated in the liver (more than 3.5-fold), moderately in the gill, kidney, and spleen (ranging from 1.5- to 2.5-fold), and barely in the brain and intestine. Results of this study could form a useful basis to explore the metal-related stress physiology of this endangered fish species.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.2
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• pp.267-272
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• 2017

Piceatannol (PIC) is a natural hydroxylated analog of resveratrol (RSV), which is a polyphenol known to extend lifespan by stimulating sirtuins. The aim of this study was to investigate the effects of PIC and RSV on the toll-like receptor 4 (TLR4)-nuclear factor kappa B ($NF-{\kappa}B$) pathway in mouse hepatocytes and an obese/diabetic KK/HlJ mouse model. AML12 mouse hepatocytes in the absence or presence of palmitic acids (PA) were treated with PIC ($50{\mu}M$) or RSV ($50{\mu}M$). Male KK/HlJ mice at 20 weeks of age were divided into three subgroups as follows: 1) obese and diabetic control (KK), 2) KK_PIC, and 3) KK_RSV. PIC and RSV were administered orally at a dose of 10 mg/kg/d for 4 weeks. Four weeks of PIC and RSV treatment did not affect body weight or food intake in KK mice. Serum fasting blood glucose was significantly reduced in KK_PIC, and 2 h oral glucose tolerance test area under the curve was significantly reduced by PIC and RSV treatment in KK mice. PIC tended to improve homeostasis model assessment of the insulin resistance index (HOMA-IR) and HOMA beta-cells in diabetic KK mice. TLR4 and $NF-{\kappa}B$ were down-regulated by PIC and RSV treatments in hepatocytes in the absence or presence of PA. Insulin receptor, AMP-activated protein kinase, peroxisome proliferator-activated receptor gamma, nucleotide oligomerization domain-like receptor family pyrin domain-containing 3, interleukin-1, and $NF-{\kappa}B$ were altered in PIC-treated livers. Collectively, PIC and RSV inhibited the $TLR4-NF-{\kappa}B$ pathway, and PIC seems to be more effective than RSV in the regulation of analyzed targets, which are involved in insulin signaling and inflammation in vivo.

• Journal of Life Science
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• v.28 no.1
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• pp.43-49
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• 2018

Chrysoeriol is a widespread flavone, and it is usually found in alfalfa, which has been used as a traditional medicine to treat dyspepsia, asthma, and urinary system disorders. Recently, analysis has been conducted on the anti-inflammatory activity of chrysoeriol, but information on its antioxidative capacity is limited. In this study, the antioxidative potential of chrysoeriol against oxidative damage and its molecular mechanisms were evaluated by analysis of the cell viability, reactive oxygen species (ROS) formation, and Western blots in the RAW 264.7 cell line. Chrysoeriol significantly scavenged lipopolysaccharide (LPS)-induced intracellular ROS formation in a dose-dependent manner, without any cytotoxicity. Heme oxygenase-1 (HO-1), a phase II enzyme that exerts antioxidative activity, was also potently induced by chrysoeriol treatment, which corresponded to the translocation of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) into the nucleus. Moreover, mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) were analyzed due to their important role in maintaining cellular redox homeostasis against oxidative stress. As a result, chrysoeriol-induced HO-1 upregulation was mediated by extracellular signal - regulated kinase (ERK), c-Jun $NH_2$-terminal kinase (JNK), and p38 phosphorylation. To identify the antioxidative potential exerted by HO-1, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was applied and mitigated by chrysoeriol treatment, which was confirmed by the HO-1 selective inhibitor and inducer, respectively. Consequently, chrysoeriol strongly strengthened the HO-1-mediated antioxidative potential through the regulation of the Nrf2/MAPK signaling pathways.

• Applied Microscopy
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• v.38 no.1
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• pp.29-34
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• 2008

Small amounts of zinc ions regulate a plentitude of enzymatic proteins, receptors and transcription factors, thus cells need accurate homeostasis of zinc ions. Some neurons have developed mechanisms to accumulate zinc in specific membrane compartment ("vesicular zinc"), which can be evidenced using histochemical techniques. These neurons are the socalled zinc enriched (ZEN) neurons, which accumulate glutamate and zinc inside their synaptic vesicles and release it during synaptic transmission. In the present paper we have studied the distribution of the ZEN terminals in the rat hippo-campus using ZnSe autometallography, Neo-Timm staining, ZnT3 immunohistochemistry and TSQ fluorescence staining.

• Child Health Nursing Research
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• v.7 no.4
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• pp.494-510
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• 2001

As a family respond to any stressful situation as a whole system, cancer diagnosis of a child, as a serious life event, could be emotional shock to destroy homeostasis of the family system. A family has a resilient capacity to adjust and adapt to stressful events. Previous studies have been focused on family stress and adaptation, but little attention has been given to family value as one of resilient factors. The data for model testing were collected from July 18, 2000 to August 30, 2000 and the analysis included 309 parents of children who are diagnosed as cancer, 18 or less years of age, and treated either hospitalized or at the outpatient clinics. The data analysis utilized SAS 6.12 and LISREL 8 for descriptive statistics, correlation, cluster analysis, factor analysis, and LISREL. The study findings are as follows. 1) Monthly income (γ=-0.28, t=-5.81) was the most important factor to explain family strain along with family support (γ=-0.11, t=-2.43), severity of children's illness (γ=0.26, t=5.22), and family stressor (γ=0.22, t=4.62). All of these factors together explained 40％ of variance in family strain. 2) Among general family value, the relationship with the parents (γ=0.28, t=4.89) and relationship with the children (γ=0.20, t=3.60) showed positive effects to family value for cancer children, while relationship with the spouse (γ=-0.19, t=-3.22) and the age of the cancer children (γ=-0.11, t=-2.21) showed negative effects. These predictors together explained 22％ of variance in family value for cancer children. 3) Family hardiness was explained mostly by family strain (γ=-0.53, t=-8.65) along with direct negative effects of family persistency and indirect negative effects of severity of children's illness, family stressor, relationship with the spouse, and the children's age. Family value for cancer children was the most important predictor with positive effect (γ=0.44, t=6.76) along with indirect effects of monthly income, relationship with the parents, relationship with the children, support from family and significant others, and confidence with the health professionals. 51％ of variance in family hardiness was explained by all of these predictors. 4) The most important predictor for family adaptation was family stressor (γ=-0.50, t=-6.85) with direct and indirect negative effects along with the severity of children's illness (γ=-0.27, t=-5.21). However, family value for cancer children showed compromised total effect (γ=-0.13, t=-1.99) with negative direct effects (γ=-0.28, t=-3.43) and positive indirect effects (γ=0.14, t=3.01). Similarly, confidence with the health professionals also showed compromised total effect (γ=0.09, t=1.99) with positive direct effects and negative indirect effects. Family hardiness showed the biggest positive direct effects while other factors such as monthly income, family stressor, family persistence, support of family and significant others, relationship with the parents, relationship with the children, and relationship with the spouse, and children's age showed indirect effects only. 39％ of variance in family adaptation was explained by all of these predictors.

• Journal of Life Science
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• v.25 no.3
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• pp.317-322
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• 2015

Alcohol-induced fatty liver (steatosis) results from excessive generation of reducing equivalents by ethanol metabolism. Generally, chronic ethanol treatment causes hepatosteatosis by regulating sterol regulatory element-binding protein 1c (SREBP-1c), which increases the synthesis of hepatic lipids. The effect of ethanol on SREBP-1c is mediated through mammalian sirtuin-1 (SIRT-1), a NAD⁺-dependent protein deacetylase that regulates hepatic lipid metabolism. Ginseng is a widely used herbal medicine that is used in Asia for its anti-diabetes and anti-obesity effects. The pharmacological and therapeutic effects of ginseng are primarily produced by bioactive constituents known as ginsenosides. Here, we examined the regulatory effects of Korean red ginseng (KRG) extracts on SREBP-1c and SIRT-1 on lipid homeostasis in AML-12 mouse hepatocytes. AML-12 cells were treated with ethanol and/or KRG extracts (0 - 1,000 μg/ml). Lipid droplets were assayed using Oil red O staining, and western blotting was used to measure SIRT-1 and SREBP-1 expression. Treatment with KRG extracts restored SIRT-1 expression and reduced SREBP-1c expression in ethanol-treated cells. We also showed that KRG extract and ginsenosides Rb₂ and Rd significantly decreased SREBP-1 acetylation in ethanol-treated cells. These results show that treatment with KRG extract and its active ginsenoside constituents Rb₂ and Rd protected against alcohol-related hepatosteatosis via regulation of SIRT-1 and downstream acetylation of SREBP-1c, which altered hepatic lipid metabolism.

• Korean Journal of Agricultural and Forest Meteorology
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• v.13 no.3
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• pp.140-147
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• 2011

We studied the influence of livestock waste leachate on oxidative damage and antioxidative responses in poplar clones in August which increase the demand of antioxidants because of high temperature and high light during this period. We measured ion leakage, antioxidant enzyme activities (APX, GR), and carotenoid contents. Oxidative damage and antioxidative responses by treated livestock waste leachate in poplar clones showed various results. We divided poplar clones into three groups using the criteria based on ion leakage which represent cell damage induced oxidative stress. Eco 28, 62-10, Bonghwa1 and Dorskamp belonged to the first group in which the cell damaged level was lower than that of the control. The results suggest that this group augmented for demand of antioxidative in summer because high concentration of nitrogen induced by treatment of live stock wastes acted as environmental stress. Consequently, they failed to keep up the homeostasis of reactive oxygen species. The second group in which the cell damaged level was similar to that of the control was Suwon, 72-30 and 72-31 clones. Finally, 97-18 clone belonged to the third group in which the cell damaged level was lower than that of the control group. In this case, nitrogen treated by livestock waste leakage decreased oxidative stress. 97-18 clone was the clones with the least damage in summer oxidative stresses treated by livestock waste leakage. These results suggest that the high concentration nitrogen due to the livestock waste leakage can act differently upon the clones. We speculate that the added oxidation damage in the summer (growing season) may have an effect on the total fresh weight and also influence the purification ability for livestock waste leakage. However, further studies are needed for the confirmation.

• Journal of Plant Biotechnology
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• v.37 no.4
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• pp.549-555
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• 2010

Here we focused on tip-burn and blossom-end rot (BER) symptoms in the tomato plants expressing the constitutively active form of $Ca^{2+}/H^+$ antiporter (sCAX1) and/or a Ca-binding protein (calreticulin, CRT) genes during their whole growth period. Conclusively we demonstrated that CRT is able to suppress the tip-burn and BER symptoms that were induced by sCAX1. Under poor nutrition condition, tomato plants overexpressing sCAX1 showed severe necrotic collapses in both roots and shoot polar tissues, which are in accordance with $Ca^{2+}$ deficient symptoms frequently observed in an agricultural cultivation of tomato. Reciprocal grafting trials using sCAX1 and wild type plants revealed that the tip-burn symptom by sCAX1 overexpression is not caused by hindrance of $Ca^{2+}$ uptake from soil. We constructed CRT overexpressing transgenic tomatoes, and crossed them with sCAX1 transgenic plants to investigate the effects of CRT on the symptoms of sCAX1 transgenic plants. Co-expression of sCAX1 and CRT significantly suppressed the $Ca^{2+}$ deficient symptoms of sCAX1 transgenic plants. Those results suggest the model that $Ca^{2+}$ homeostasis disturbed by the overexpression of sCAX1 may be suppressed by the co-expression of CRT.

• Journal of Ginseng Research
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• v.46 no.6
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• pp.780-789
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• 2022

Background: Incretin impairment, characterized by insufficient secretion of L-cell-derived glucagon-like peptide-1 (GLP-1), is a defining step of type 2 diabetes mellitus (T2DM). Ginsenoside compound K (CK) can stimulate GLP-1 secretion; however, the potential mechanism underlying this effect has not been established. Methods: CK (40 mg/kg) was administered orally to male db/db mice for 4 weeks. The body weight, oral glucose tolerance, GLP-1 secretion, gut microbiota sequencing, bile acid (BA) profiles, and BA synthesis markers of each subject were then analyzed. Moreover, TGR5 expression was evaluated by immunoblotting and immunofluorescence, and L-cell lineage markers involved in L-cell abundance were analyzed. Results: CK ameliorated obesity and impaired glucose tolerance in db/db mice by altering the gut microbiota, especially Ruminococcaceae family, and this changed microbe was positively correlated with secondary BA synthesis. Additionally, CK treatment resulted in the up-regulation of CYP7B1 and CYP27A1 and the down-regulation of CYP8B1, thereby shifting BA biosynthesis from the classical pathway to the alternative pathway. CK altered the BA pool by mainly increasing LCA and DCA. Furthermore, CK induced L-cell number expansion leading to enhanced GLP-1 release through TGR5 activation. These increases were supported by the upregulation of genes governing GLP-1 secretion and L-cell differentiation. Conclusions: The results indicate that CK improves glucose homeostasis by increasing L-cell numbers, which enhances GLP-1 release through a mechanism partially mediated by the gut microbiota-BA-TGR5 pathway. Therefore, that therapeutic attempts with CK might be useful for patients with T2DM.

• Journal of Life Science
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• v.27 no.8
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• pp.958-964
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• 2017

Autophagy plays an important role in cellular homeostasis and survival for cell recycling and various stresses within the cell. Recent studies have shown that autophagy activity modulates the expression of oncogene and tumor suppressor genes, leading to the development or suppression of cancer. Induction of autophagy is involved in preventing cancer development in normal cells and plays an important role in prompting a specific cell death mechanism in cancer cells with damaged cell death function. It is also known that autophagy inhibition increases the therapeutic efficacy by sensitizing cancer cells that are resistant to chemotherapy. However, the role of autophagy has not yet been fully understood in cancer treatment. Oral squamous cell carcinoma accounts for more than 90% of oral cancer and is the sixth most common cancer in the world. The incidence of oral cancer has increased by 50% over the last 20 years and the mortality rate is over 40% within 5 years after the onset. In oral cancers, the role of autophagy are described to look for tumor inhibitory in the early stages of tumor formation, like other cancers, indicating the dual functions involved in tumor cell survival include tumor progression stages. This review summarizes the various roles of autophagy in cancer cells and suggests the possibility of autophagy as a promising target for effective oral cancer therapy.