• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.6
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• pp.832-841
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• 2013

This research, as a basic preliminary study for development of functional health food, is aimed at assessing the body fat reduction effect and for application to human body for such reduction in actual clinical settings by preliminary extraction of 2 types of wild edible greens, Lythrum salicaria L. and Aceriphyllum rossii. Subjects over the age of 19 and less than 60 years old with BMI value range of $23.0kg/m^2{\sim}29.9kg/m^2$ were recruited through screening were divided into experimental group and control group, each with 25 subjects, through randomized allocation. With both patients and evaluators wearing blindfold, the experimental group was orally administered with 4 capsules of 500mg of composite preparation containing the extracts of Lythrum salicaria L. and Aceriphyllum rossii 3 times a day for a period of 8 weeks while the control group was orally administered with 4 capsules of 500mg of placebo (fake food) with the same appearance as the preparation administered to the experimental group 3 times a day for a period of 8 weeks. After having carried out evaluation on physical examinations (body weight, BMI and body fat ratio, etc.), laboratory tests (general blood test, biochemical test of blood and urine test), lipid test, the changes were analyzed. There was no significant change between the 2 groups and within the groups in BMI and body fat ratio, which are the primary effectiveness evaluation at each time. There was no significant difference between the 2 groups in serum lipid and WHR, obesity related KOQOL, KEAT-26 which are the secondary effectiveness evaluations. There was no change between the 2 groups and within the groups in vital sign, CBC, BC and urin test. These results suggest that Lythrum salicaria L. and Aceriphyllum rossii ext. showed no significant reduction in BMI, body fat ratio and serum lipid. Additional confirmative clinical application test is needed in the future.

• Journal of Microbiology and Biotechnology
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• v.15 no.4
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• pp.756-766
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• 2005

The signaling mechanism underlying aburatubolactam C-induced FasL upregulation was investigated in human Jurkat T cells. After treatment with aburatubolactam C, the src-family PTKs $p56^{lck}\;and\;p59^{fyn}$, and MAP kinases ERK2 and JNK1, were activated prior to FasL upregulation; Both $p56^{lck}\;and\;p59^{fyn}$ were directly activated 2.4- and 2.2-fold, respectively, in vitro by aburatubolactam C. The aburatubolactam C-induced cellular changes, including the activation of ERK2 and INK1, and FasL upregulation, were completely prevented by the PTK inhibitor genistein. The activation of protein kinase C (PKC$\delta,\;\epsilon\;and\;\mu$ was also induced following aburatubolactam C treatment. Although the activation of $p56^{lck}$ and tyrosine phosphorylation of the cellular proteins were not blocked by the PKC inhibitor GFl09203X, the activation of ERK2 was completely abrogated, along with a detectably enhanced JNK1 activation; FasL upregulation, and apoptosis. However, the FasL upregulation and apoptosis were significantly inhibited by the PKC activator PMA, with a remarkable increase in the ERK2 activation. The cytotoxic effect of aburatubolactam C was reduced in the presence of the anti-Fas neutralizing antibody ZB-4. Although ectopic expression of Bcl-2 failed to completely block the cytotoxicity of aburatubolactam C, it was clearly suppressed. The c-Fos mRNA expression was upregulated in a biphasic manner, where the second phasic expression overlapped with the FasL upregulation. Accordingly, these results demonstrate that aburatubolactam C-induced apoptosis is exerted, at least in part, by FasL upregulation dictated by activation of the PTK ($p56^{lck}\;and\;p59^{fyn}$) /JNKI pathway, which is negatively affected by the concurrent activation of the PKC/ERK2 pathway proximal to PTK activation.

• Journal of Embryo Transfer
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• v.26 no.2
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• pp.97-104
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• 2011

This study was carried out to confirm the effects of luteotrophin, human chorionic gonadotrophin (hCG), and an anti-luteolytic agent, flunixin meglumin (FM), on pregnancy rates in Hanwoo with in vitro produced (IVP) embryo transfers (ET), and to research the effects on the estrus cycle. Treatments included hCG and FM administration 3~10 minutes prior to ET. Also, pregnancy rates were compared with lidocane treatment and FM treatment prior to ET. The results are shown below. 30-day pregnancy rate was 76.7% in the hCG-treated group and 75.7% in the FM-treated group. Both rates were higher than the 70% rate for the control group. 42-day pregnancy rate was 76.7% in the FM-treated group. This was higher than 66.7% recorded for both the hCG-treated and control groups. The pregnancy rate of the hCG-treated group was high at Day 30 (76.7%) but low at Day 40 (66.7%), and there were no differences from the FM-treated and control groups. The recurrent estrus rate of infertile individuals at 2 weeks after ET was 36.4% in the hCG-treated group, under 71.4% in the FM-treated group and 80.0% in the control group. The non-pregnancy rate of individuals without recurrent estrus was 18.2% in the hCG-treated group, which was higher than the 0% rate in both the FM-treated and control groups. The pregnancy rates were higher in the FM-treated group than the Lidocane-treated group with 72.3% versus 67.5% in the heifers and 48.9% versus 43.6% in the cows. From the above results, the FM treatment proved more effective than the hCG treatment and no treatment whatsoever in increasing pregnancy rates after ET. In addition, hCG treatment was shown to be undesirable due to the deviations it caused in the reproductive physiology of the hCG-treated recipients. Therefore, in our study, the FM treatment resulted in a higher pregnancy rate than either lidocaine treatment or no-treatment in the trials of ET.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.1
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• pp.1-7
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• 2011

Many anticancer agents as well as ionizing radiation have been shown to induce autophagy which is originally described as a protein recycling process and recently reported to play a crucial role in various disorders. In HCT116 human colon cancer cells, we found that curcumin, a polyphenolic phytochemical extracted from the plant Curcuma longa, markedly induced the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and degradation of sequestome-1 (SQSTM1) which is a marker of autophagosome degradation. Moreover, we found that curcumin caused GFP-LC3 formation puncta, a marker of autophagosome, and decrease of GFP-LC3 and SQSTM1 protein level in GFP-LC3 expressing HCT116 cells. It was further confirmed that treatment of cells with hydrogen peroxide induced increase of LC3 conversion and decrease of GFP-LC3 and SQSTM1 levels, but these changes by curcumin were almost completely blocked in the presence of antioxidant, N-acetylcystein (NAC), indicating that curcumin leads to reactive oxygen species (ROS) production, which results in autophagosome development and autolysosomal degradation. In parallel with NAC, SQSTM1 degradation was also diminished by bafilomycin A, a potent inhibitor of autophagosome-lysosome fusion, and cell viability assay was further confirmed that cucurmin-induced cell death was partially blocked by bafilomycin A as well as NAC. We also observed that NAC abolished curcumin-induced activation of extracelluar signal-regulated kinases (ERK) 112 and p38 mitogen-activated protein kinases (MAPK), but not Jun N-terminal kinase (JNK). However, the activation of ERK1/2 and p38 MAPK seemed to have no effect on the curcumin-induced autophagy, since both the conversion of LC3 protein and SQSTM1 degradation by curcumin was not changed in the presence of NAC. Taken together, our data suggest that curcumin induced ROS production, which resulted in autophagic activation and concomitant cell death in HCT116 human colon cancer cell. However, ROS-dependent activation of ERK1/2 and p38 MAPK, but not JNK, might not be involved in the curcumin-induced autophagy.

• Clinical and Experimental Pediatrics
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• v.46 no.4
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• pp.335-339
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• 2003

Purpose : Surfactant protein A(SP-A) is involved in surfactant physiology and structure, and plays a major role in innate host defense and inflammatory processes in the lung. Steroid therapy is widely used for mothers who threaten to deliver prematurely and also used commonly in the management of preterm infants with chronic lung disease. Two SP-A genes(SP-A1, SP-A2) and several alleles have been characterized for each SP-A gene in human. Preliminary evidence indicates that differences may exist among alleles in response to Dexamethasone(Dexa) and that the SP-A 3'UTR plays a role in this process. We studied whether 3'UTR-mediated differences exist among the most frequently found SP-A alleles in response to Dexa. Methods : Constructs containing the 3'UTR from eight different SP-A alleles were made using luciferase as a the reporter gene. These constructs were driven by the SV40 promotor and were transfected along with a transfection control vector in H441 cells that express SP-A. The activity of the reporter gene in the presence or absence of Dexa(100 nM) treatment was measured. All the experiments for the eight SP-A alleles studied, were performed in triplicate and repeated five times. The results were normalized to the transfection control. Results : Expression of alleles of 6A3, 6A, 1A were significantly decreased in response to Dexa. Conclusion : Three UTR mediated differences exist among human SP-A variants both in the basal expression and in response to Dexa. These genotype-dependent differences may point to a need for a careful consideration of individual use of steroid treatment in the prematurely born infant.

• Nutrition Research and Practice
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• v.9 no.4
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• pp.379-384
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• 2015

BACKGROUND/OBJECTIVE: Apolipoprotein A5 gene promoter region T-1131C polymorphism (APOA5 T-1131C) is known to be associated with elevated plasma TG levels, although little is known of the influence of the interaction between APOA5 T-1131C and lifestyle modification on TG levels. To investigate this matter, we studied APOA5 T-1131C and plasma TG levels of subjects participating in a three-month lifestyle modification program. SUBJECTS/METHODS: A three-month lifestyle modification program was conducted with 297 participants (Age: $57{\pm}8years$) in Izumo City, Japan, from 2001-2007. Changes in energy balance (the difference between energy intake and energy expenditure) and BMI were used to evaluate the participants' responses to the lifestyle modification. RESULTS: Even after adjusting for confounding factors, plasma TG levels were significantly different at baseline among three genotype subgroups: TT, $126{\pm}68mg/dl$; TC, $134{\pm}74mg/dl$; and CC, $172{\pm}101mg/dl$. Lifestyle modification resulted in significant reductions in plasma TG levels in the TT, TC, and CC genotype subgroups: $-21.9{\pm}61.0mg/dl$, $-20.9{\pm}51.0mg/dl$, and $-42.6{\pm}78.5mg/dl$, respectively, with no significant differences between them. In a stepwise regression analysis, age, APOA5 T-1131C, body mass index (BMI), homeostasis model assessment-insulin resistance (HOMA-IR), and the 18:1/18:0 ratio showed independent association with plasma TG levels at baseline. In a general linear model analysis, APOA5 T-1131C C-allele carriers showed significantly greater TG reduction with decreased energy balance than wild type carriers after adjustment for age, gender, and baseline plasma TG levels. CONCLUSIONS: The genetic effects of APOA5 T-1131C independently affected plasma TG levels. However, lifestyle modification was effective in significantly reducing plasma TG levels despite the APOA5 T-1131C genotype background.

• Journal of Microbiology and Biotechnology
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• v.12 no.1
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• pp.121-129
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• 2002

Using recombinant Chinese hamster ovary (CHO) cells, strategies for developing high producers for the recombinant human Transforming Growth $Factor-{\beta}1$ ($TGF-{\beta}1$) protein are proposed and their physiological characteristics in cell cultures were investigated. $TGF-{\beta}1$ is a pleiotrophic polypeptide involved in various biological activities, including cell growth, differentiation, and deposition of extracellular matrix proteins. The CHO cells included human $TGF-{\beta}1$ cDNA in conjunction with a dihydrofolate reductase (DHFR) gene, which was cotransfected into the cells to amplify the transfected $TGF-{\beta}1$ cDNA. As a first-round screening of the transfected cells, a relatively high $TGF-{\beta}1$-producing cell line was selected, and then, it acquired a resistance to increasing concentrations of methotrexate (MTX) up to $60{\mu}M$,resulting in a significant improvement in its $TGF-{\beta}1$ biosynthetic ability. After applying a monoclonal selection strategy to the MTX-resistant cells, more productive cells were screened, including the APP-3, App-5, and App-8 cell lines. These high producers were compared with two other cell lines (AP-l cell line without amplification of transfected $TGF-{\beta}1$ cDNA and nontransfectant of $TGF-{\beta}1$ cDNA) in terms of cell growth, $TGF-{\beta}1$ productivity, sugar uptake, and byproduct formation, in the presence or absence of MTX in the culture medium. Consequently, both monoclonal selection as well as an investigation of the physiological characteristics were found to be needed for the efficient screening of higher $TGF-{\beta}1$ producers, even after the transfection and amplification of the transfected gene.

• BMB Reports
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• v.51 no.10
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• pp.532-537
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• 2018

Prostaglandin $E_2$ ($PGE_2$), a major product of cyclooxygenase-2 (COX-2), plays an important role in the carcinogenesis of many solid tumors, including colorectal cancer. Because $PGE_2$ functions by signaling through $PGE_2$ receptors (EPs), which regulate tumor cell growth, invasion, and migration, there has been a growing amount of interest in the therapeutic potential of targeting EPs. In the present study, we investigated the role of EP4 on the effectiveness of cordycepin in inhibiting the migration and invasion of HCT116 human colorectal carcinoma cells. Our data indicate that cordycepin suppressed lipopolysaccharide (LPS)-enhanced cell migration and invasion through the inactivation of matrix metalloproteinase (MMP)-9 as well as the down-regulation of COX-2 expression and $PGE_2$ production. These events were shown to be associated with the inactivation of EP4 and activation of AMP-activated protein kinase (AMPK). Moreover, the EP4 antagonist AH23848 prevented LPS-induced MMP-9 expression and cell invasion in HCT116 cells. However, the AMPK inhibitor, compound C, as well as AMPK knockdown via siRNA, attenuated the cordycepin-induced inhibition of EP4 expression. Cordycepin treatment also reduced the activation of CREB. These findings indicate that cordycepin suppresses the migration and invasion of HCT116 cells through modulating EP4 expression and the AMPK-CREB signaling pathway. Therefore, cordycepin has the potential to serve as a potent anti-cancer agent in therapeutic strategies against colorectal cancer metastasis.

• Molecules and Cells
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• v.24 no.1
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• pp.95-104
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• 2007

The mechanism of acacetin-induced apoptosis of human breast cancer MCF-7 cells was investigated. Acacetin caused 50% growth inhibition ($IC_{50}$) of MCF-7 cells at $26.4{\pm}0.7{\mu}M$ over 24 h in the MTT assay. Apoptosis was characterized by DNA fragmentation and an increase of sub-G1 cells and involved activation of caspase-7 and PARP (poly-ADP-ribose polymerase). Maximum caspase 7 activity was observed with $100{\mu}M$ acacetin for 24 h. Caspase 8 and 9 activation cascades mediated the activation of caspase 7. Acacetin caused a reduction of Bcl-2 expression leading to an increase of the Bax:Bcl-2 ratio. It also caused a loss of mitochondrial membrane potential that induced release of cytochrome c and apoptosis inducing factor (AIF) into the cytoplasm, enhancing ROS generation and subsequently resulting in apoptosis. Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF. Stress-activated protein kinase/c-Jun $NH_4$-terminal kinase 1/2 (SAPK/JNK1/2) and c-Jun were activated by acacetin but extracellular-regulated kinase 1/2 (Erk1/2) nor p38 mitogen-activated protein kinase (MAPK) were not. Our results show that acacetin-induced apoptosis of MCF-7 cells is mediated by caspase activation cascades, ROS generation, mitochondria-mediated cell death signaling and the SAPK/JNK1/2-c-Jun signaling pathway, activated by acacetin-induced ROS generation.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1075-1081
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• 2007

We investigated whether 1) capsaicin ingestion (100 mg) enhances autonomic nervous system (ANS) activities associated with thermogenic sympathetic activity as energy metabolic modulator, 2) UCP1 and ${\beta}_{3}$-AR variants of each subjects influence with ANS activity. Eight healthy males (24.7 ${\pm}$ 1.8 yr) volunteered for this study. The cardiac autonomic nervous activities evaluated by means of heart rate variability of power spectral analysis and energy metabolism were continuously measured during 5-min rest for total 90-min resting condition with placebo or capsaicin oral administration chosen at random. The results indicated that there were no significant differences in heart rate during rest between both trials. Autonomic nervous activity increased in capsaicin tablet trial, but the difference did not reach the statistical significance. Capsaicin, however, induced significantly lower respiratory gas exchange ratio at Test3 (CAP: 0.80 ${\pm}$ 0.02 vs. 0.85 ${\pm}$ 0.02), means ${\pm}$ SE, p<0.05). In conclusion, it may be suggested the capsaicin consumption as a valuable supplement for the treatment of individual with hyperlipidemia and/or obesity by improving lipolysis. Further studies will also be considered genetic variants such as UCP1 and/or ${\beta}_{3}$-AR associated with obesity.