• Journal of Digital Convergence
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• v.18 no.3
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• pp.267-273
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• 2020

To determine the biological effects of exercise on hippocampus in mice brain exposed to radiofrequency radiaton (RF), the expression of AMPKα, p-AMPKα, ERK1/2, p-ERK1/2, p38, and p-p38 protein in the mouse exposed to RF were investigated in the hippocampal tissues, Western blot method was used to compare the protein expression levels for each molecule. Significant increases in protein expression of individual and phosphorylated molecules were observed in the spontaneous exercise group, and the expression of these molecules was notably decreased in the RF exposure and spontaneous exercise group. This study shows that neuroplasticity can be increased by exercise in hippocampus that is responsible for memory, but memory and cognitive function may be affected by exposure to RF. We may expect clinically interesting results on dementia or Alzheimer disease if we proceed further investigation on the effect of RF.

• Journal of Photoscience
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• v.9 no.2
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• pp.229-232
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• 2002

There are two distinct UV-responsive signaling pathways in UV-irradiated mammalian cells, i.e., the DNA damage-dependent and -independent pathways. The former occurs in nucleus and results in growth arrest and apoptosis via post-translational modification of p53. The latter is initiated by oxidative stress and/or by damages in cell membrane or cytoplasm, which activate signaling cascade through intracellular molecules including mitogen activated protein kinases (MAPK). In normal human fibroblastic cells, all of MAPK family members, extracellular signal-related kinases (ERK), c-Jun N-terminal kinases (JNK) and p38, were rapidly phosphorylated following UV-irradiation. ERK phosphorylation was suppressed by an inhibitor of receptor tyrosine kinases (RTK). As ERK usually responds to mitogenic stimuli from RTK ligands, UV-induced ERK phosphorylation may be linked to the proliferation of survived cells. In contrast, phosphorylation of JNK and p38, as well as apoptosis, were modulated by the level of UV-generated oxidative stress Therefore, JNK and p38 may take part in oxidative stress-mediated apoptosis. Phosphorylation of p53 at Ser and Thr residues are essential for stabilization and activation of p53. Among several sites reported, we confirmed phosphorylation at Ser-15 and Ser-392 after UV-irradiation. Both of these were inhibited by a phosphoinositide 3-kinase inhibitor, presumably due to the shutdown of signals from DNA damage to p53. Phosphorylation at Ser-392 was also sensitive to an antioxidant and a p38 inhibitor, suggesting that Ser-392 of p53 is one of the possible points where DNA damage-dependent and -independent apoptic signals merge. Thus, MAPK pathway links UV-induced intracellular signals to the nuclear responses and modifies DNA damage-dependent cellular outcome, resulting in the determination of cell death.

• Women's Health Nursing
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• v.20 no.1
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• pp.38-47
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• 2014

Purpose: This study aimed to identify related factors of prenatal depression by stress-vulnerability and stress-coping models for pregnant women. Methods: A cross-sectional survey design with a convenience sampling was used. A total of 107 pregnant women who visited a general hospital in a metropolitan city were recruited from August to October, 2013. A structured questionnaire included the Korean version of Beck Depression Inventory II, and the instruments measuring Self-Esteem, Marital Satisfaction, Pregnancy Stress, Stressful Life Events, and Coping. The data were analyzed using descriptive statistics, t-test, Parson's correlation analysis, and stepwise multiple regression. Results: The mean score of prenatal depression was $11.95{\pm}6.2$, then showing 19.6% with mild depression, 15.0% with moderate depression, and 0.9% with severe depression on BDI II scale. Prenatal depression had positive correlation with pregnancy stress (r=.55, p<.01), stressful life events (r=.26, p<.01) and negative correlation with self- esteem (r=-.38, p<.01), marital satisfaction (r=-.40, p<.01), and coping (r=-.21, p<.05). Factors of pregnancy stress, self-esteem, stressful life events, and planned pregnancy explained 38% of the total variance of prenatal depression. Conclusion: These findings show that health providers need to assess prenatal depression and to control the influencing factors.

• Biomolecules & Therapeutics
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• v.32 no.2
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• pp.214-223
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• 2024

Metabolic abnormalities in the liver are closely associated with diverse metabolic diseases such as non-alcoholic fatty liver disease, type 2 diabetes, and obesity. The aim of this study was to evaluate the ameliorating effect of robinetin (RBN) on the significant pathogenic features of metabolic failure in the liver and to identify the underlying molecular mechanism. RBN significantly decreased triglyceride (TG) accumulation by downregulating lipogenesis-related transcription factors in AML-12 murine hepatocyte cell line. In addition, mice fed with Western diet (WD) containing 0.025% or 0.05% RBN showed reduced liver mass and lipid droplet size, as well as improved plasma insulin levels and homeostatic model assessment of insulin resistance (HOMA-IR) values. CD38 was identified as a target of RBN using the BioAssay database, and its expression was increased in OPA-treated AML-12 cells and liver tissues of WD-fed mice. Furthermore, RBN elicited these effects through its anti-histone acetyltransferase (HAT) activity. Computational simulation revealed that RBN can dock into the HAT domain pocket of p300, a histone acetyltransferase, which leads to the abrogation of its catalytic activity. Additionally, knock-down of p300 using siRNA reduced CD38 expression. The chromatin immunoprecipitation (ChIP) assay showed that p300 occupancy on the promoter region of CD38 was significantly decreased, and H3K9 acetylation levels were diminished in lipid-accumulated AML-12 cells treated with RBN. RBN improves the pathogenic features of metabolic failure by suppressing the p300-CD38 axis through its anti-HAT activity, which suggests that RBN can be used as a new phytoceutical candidate for preventing or improving this condition.

• Journal of Nutrition and Health
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• v.38 no.2
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• pp.151-160
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• 2005

The purpose of this study was to compare the mineral status of postmenopausal vegetarian women with those of the omnivores, and to investigate the relationship between dietary pattern and minerals status in postmenopausal Korean women. The research group was composed of vegetarian women (n = 38), all of them were seven day adventists, who had been on vegetarian diet over 20 yrs. Their anthropometric measurements, dietary intakes, and blood mineral concentrations were compared to age matched omnivores controls (n = 38). The average age of vegetarians and omnivores were 60.7 yrs and 60.5 yrs, respectively and there was no significant difference. The mean daily energy intake of vegetarians and omnivores were 1518.5 kcal and 1355.5 kcal, respectively and their was no significant difference. The mean calcium intake of vegetarians (492.6 mg) was not significantly different from that of omnivores (436.6 mg). The vegetarians consumed significantly greater quantities of magnesium (p < 0.001), iron (p < 0.001), copper (p < 0.001), manganese (p < 0.001) and dietary fiber (p < 0.05). There were no significantly differences in serum calcium, magnesium and manganese levels between vegetarians and omnivores. However, serum levels of phosphorus (p < 0.01), iron (p < 0.05), ferritin (p < 0.01), zinc (p < 0.001) and copper (p < 0.05) were significantly lower than those of omnivores. In conclusion, vegetarian postmenopausal women may have low bioavailability of iron, zinc and copper. Therefore it was needed that further study on mineral bioavailability of vegetarian diet. (Korean J Nutrition 38(2): 151～160, 2005)

• The korean journal of orthodontics
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• v.33 no.3 s.98
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• pp.169-183
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• 2003

Tooth movement by orthodontic force effects great tissue changes within the periodontium, especially by shifting the blood flow in the pressure side and resulting in a hypoxic state of low oxygen tension. The aim of this study is to elucidate the possible mechanism of apoptosis in response to hypoxia in MC3T3El osteoblasts, the main cells in bone remodeling during orthodontic tooth movement. MC3T3El osteoblasts under hypoxic conditions ($2\%$ orygen) resulted in apoptosis in a time-dependent manner as estimated by DNA fragmentation assay and nuclear morphology stained with fluorescent dye, Hoechst 33258. Pretreatment with Z-VAD-FMK, a pancaspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to hypoxia. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-1 activity (YVADase) was detected. To confirm what caspases are involved in apoptosis, Western blot analysis was performed using anti-caspase-3 or -6 antibodies. The 10-kDa protein, corresponding to the active products of caspase-3, and the 10-kDa protein of the active protein of caspase-6 were generated in hypoxia-challenged cells in which the processing of the full length form of caspase-3 and -6 was evident. While a time course similar to this caspase-3 and -6 activation was evident, hypoxic stress caused the cleavage of lamin A, which was typical of caspase-6 activity. In addition, the stress elicited the release of cytochrome c into the cytosol during apoptosis. Furthermore, we observed that pre-treatment with SB203580, a selective p38 mitogen activated protein kinase inhibitor, attenuated the hypoxia-induced apoptosis. The addition of SB203S80 suppressed caspase-3 and -6-like protease activity by hypoxia up to $50\%$. In contrast, PD98059 had no effect on the hypoxia-induced apoptosis. To confirm the involvement of MAP kinase, JNK/SAPK, ERK, or p38 kinase assay was performed. Although p38 MAPK was activated in response to hypoxic treatment, the other MAPK -JNK/SAPK or ERK- was either only modestly activated or not at all. These results suggest that p38 MAPK is involved in hypoxia-induced apoptosis in MC3T3El osteoblasts.

• Journal of Life Science
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• v.21 no.2
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• pp.242-250
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• 2011

Although insulin-like growth factor-I (IGF-I) and androgen receptor (AR) coactivators are well known effectors of skeletal muscle, the molecular mechanism by which signaling pathways integrating AR coactivators and IGF-I in skeletal muscle cells has not been previously examined. In this study, the effects of IGF-I treatment on the gene expression of AR coactivators in the absence of AR ligands and the roles of the p38 MAPK and ERK1/2 signaling pathways in IGF-I-induced AR coactivators induction were examined. C2C12 cells were treated with 250 ng/ml of IGF-I in the presence or absence of specific inhibitors p38 MAPK (SB203580) or ERK1/2 (PD98059). Treatment of C2C12 cells with IGF-I resulted in increased in GRIP-1, SRC-1, and ARA70 protein expression. The levels of GRIP-1, SRC-1, and ARA70 mRNA were also significantly increased after 5min of IGF-I treatment. IGF-I-induced AR coactivator proteins were significantly blocked by pharmacological inhibitors of p38 MAPK and ERK1/2 pathways. However, there was no significant effect of those inhibitors on IGF-I-induced mRNA level of AR coactivators, suggesting that AR coactivators are post-transcriptionally regulated by IGF-I. Furthermore, the present results suggest that IGF-I stimulates the expression of AR coactivators by cooperative activation of the p38 MAPK and ERK1/2 pathways in C2C12 mouse skeletal muscle cells.

• Animal cells and systems
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• v.16 no.5
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• pp.366-375
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• 2012

Gallotannin (GT) is derived from plant poly phenol and is associated with biological actions in a wide range of cells. In this study, we evaluated the effect of GTon apoptosis and cyclooxygenase-2 (COX-2) expression and attempted to shed light on the mechanism of action in A549 human lung carcinoma cells. We found that GT dramatically induced apoptosis as demonstrated by expression of p53 and active caspase-3 via western blot analysis and fragmented DNA as detected by DNA fragmentation and DAPI staining. We also observed that GT significantly causes COX-2 expression in a dose-dependent manner determined by western blot analysis. Phosphorylation of Akt and p38 was considerably increased by GT in A549 human lung carcinoma cells. Inhibition of Akt and p38kinase with LY294002 or SB203580 suppressed GT-induced apoptosis and COX-2 expression. Furthermore, we have shown that prevention of COX-2 with NS398 or indomethacin does not any effects on apoptosis induced by GT. Taken together, our present results suggest that GT regulates apoptosis and COX-2 expression through Akt and p38kinase pathway in A549, human lung carcinoma cells.

• Animal cells and systems
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• v.15 no.1
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• pp.9-17
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• 2011

Colorectal cancer is the third leading cause of cancer-related death in Western countries. Chemotherapeutic agents with different mechanisms of action have shown an increase in cure rates. In the present study, we investigated the effect of a combination of low concentration of paclitaxel (taxol, 5 nM) and topoisomerase 1 inhibitor camptothecin (CPT) on HCT116 colon cancer cells. Although the viability of cells treated with taxol alone was similar to that of control cells, sequential treatment with taxol and CPT exhibited high cytotoxicity. However, the opposite sequence of treatment did not exert cytotoxic effects on HCT116 cells. This enhanced cytotoxicity of the sequential combination therapy was the result of mitotic arrest, which increased the level of $p21^{Cip1/WAF1}$ through the p38 mitogen-activated protein kinase (MAPK) pathway. Knockdown by $p21^{Cip1/WAF1}$ siRNA or treatment with a p38 inhibitor reduced the viability of cells sequentially exposed to taxol and CPT. Taken together, a low taxol concentration in combination with CPT induced mitotic arrest in HCT116 cells, leading to synergistic cell death through enhanced expression of $p21^{Cip1/WAF1}$ and p38 MAPK pathway. Therefore, taxol could playa role as a sensitizer of CPT in colon cancer cells.

• Korean Journal of Microbiology
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• v.50 no.1
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• pp.73-83
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• 2014

The objective of the this study was to investigate the binding capacity and removal ability of lactic acid bacterial strains obtained from Korean soybean paste for mutagenic heterocyclic amines (HCAs) formed during cooking of protein-rich food at high temperature. Among 19 strains identified by carbohydrate fermentation and 16S rRNA sequencing, the live cell or cell-free culture supernatant of Lactobacillus acidophilus D11, Enterococcus faecium D12, Pediococcus acidilactici D19, L. acidophilus D38, Lactobacillus sakei D44, Enterococcus faecalis D66, and Lactobacillus plantarum D70 inhibited the mutagenesis caused by either 3-amino-1,4-dimethyl-5H-pyrido[4,3-b] indole (Trp-P-1) or 3-amino-1-methyl-5H-pyrido[4,3-b] indole (Trp-P-2) in Salmonella typhimurium TA98 and TA100. The bacterial cells of the isolated strains showed greater binding activity than the pure cell wall, exopolysaccharide, and pepetidoglycan. The carbohydrate moieties of the cell wall or protein molecules on the cell surface have a significant role in binding Trp-P-1 and Trp-P-2, since protease, heating, sodium metaperiodate, or acidic pH treatments significantly (P<0.05) reduced the binding efficacy of the tested bacteria. Addition of metal ions or sodium dodecyl sulfate decreased the binding ability of E. faecium D12, L. acidophilus D38, and E. faecalis D66. Therefore, the binding mechanisms of these strains may consist of ion-exchange and hydrophobic bonds. Especially, the high mutagen binding by L. acidophilus D38 and L. plantarum D70 may reduce the accumulation or absorption of Trp-P-1 and Trp-P-2 in the small intestine via increased excretion of a mutagen-bacteria complex.