• The Korea Journal of Herbology
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• v.33 no.6
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• pp.19-28
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• 2018

Objectives : The objective of this study was to investigate the protective effect of Flaxseed oil and Chrysanthemi Indici Flos 50% ethanol extract in an HCl/ethanol induced acute gastritis model. Methods : ICR mice were divided into 6 groups; normal mice (Nor), gastritic mice with distilled water (Veh), gastritic mice with 10 mg/kg sucralfate (SC), gastritic mice with 16 g/㎏ Flaxseed oil (FO), gastritic mice with FO + 50 mg/kg Chrysanthemi Indici Flos (FCL), and gastritic mice with FO + 100 mg/kg Chrysanthemi Indici Flos (FCH). Then, mice were orally administered with 150 mM HCl/60% ethanol and caused acute gastritis. After 1 hr, mice were sacrificed, and blood and stomach tissue were collected. Results : Administration of FCL and FCH to mice prior to the induction of gastritis was found to reduce gastric injury. reactive oxygen species (ROS) and peroxy nitrite ($ONOO^-$) levels of stomach tissues were significantly decreased in FO, FCL, and FCH compared to Veh group. As results of stomach protein analyses, FCL and FCH effectively reduce inflammatory-related factors such as inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and interleukin 1 beta ($IL-1{\beta}$) in gastric lesion mice. In addition, nuclear factor kappa B p65 ($NF-{\kappa}B$ p65) and phosphorylation inhibitor of nuclear factor kappa $B{\alpha}(p-I{\kappa}B{\alpha})$ were down-regulated in FCL and FCH administrated gastric lesion mice. Conclusions : These results suggest that FCL and FCH has an inhibitory effect against gastric injury. Therefore, FCL and FCH has the potential to be used as a natural therapeutic drug.

• Journal of Life Science
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• v.32 no.6
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• pp.482-490
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• 2022

Sarcopenia, a geriatric and multifactorial syndrome characterized by progressive systemic skeletal muscle disorder, may be associated with many comorbidities. Sarcopenia caused by a decrease in muscle mass and muscle strength is accompanied by the aggravation of various pathological conditions, and as life expectancy increases, its prevalence will continue to increase in the future. During the aging process, chronic oxidative stress and increased inflammatory responses act as major contributors to skeletal muscle loss. In addition, disruption of autophagy and apoptosis signals associated with dysfunction of mitochondria, which are essential for energy metabolism, accelerates the loss of muscle proteins. The pharmacological effect of cordycepin, a major physiologically active substance in the genus Cordyceps, which has been widely used for the prevention and treatment of various diseases for a long time, is directly related to its antioxidant and anti-inflammatory actions. In this review, we present the correlation between apoptosis, autophagy, protein catabolism, and satellite cell activity important for muscle regeneration using cordycepin for the prevention and treatment of sarcopenia. Although there have been few studies so far on the use of cordycepin for sarcopenia, previous studies suggest that cordycepin may contribute to inhibiting the age-related weakening of mitochondrial function and blocking the breakdown of muscle proteins. In addition, the protective effect of cordycepin on muscle cell damage is considered to be closely related to its antioxidant and anti-inflammatory activities. Therefore, it is considered that more continuous basic research is needed, focusing on the molecular biological mechanism of cordycepin, which is involved in the anti-aging of muscle cells.

• Biomolecules & Therapeutics
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• v.31 no.1
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• pp.73-81
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• 2023

Sirtuins (SIRTs) belong to the nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylase family. They are key regulators of cellular and physiological processes, such as cell survival, senescence, differentiation, DNA damage and stress response, cellular metabolism, and aging. SIRTs also influence carcinogenesis, making them potential targets for anticancer therapeutic strategies. In this study, we investigated the anticancer properties and underlying molecular mechanisms of a novel SIRT1 inhibitor, MHY2251, in human colorectal cancer (CRC) cells. MHY2251 reduced the viability of various human CRC cell lines, especially those with wild-type TP53. MHY2251 inhibited SIRT1 activity and SIRT1/2 protein expression, while promoting p53 acetylation, which is a target of SIRT1 in HCT116 cells. MHY2251 treatment triggered apoptosis in HCT116 cells. It increased the percentage of late apoptotic cells and the sub-G1 fraction (as detected by flow cytometric analysis) and induced DNA fragmentation. In addition, MHY2251 upregulated the expression of FasL and Fas, altered the ratio of Bax/Bcl-2, downregulated the levels of pro-caspase-8, -9, and -3 proteins, and induced subsequent poly(ADP-ribose) polymerase cleavage. The induction of apoptosis by MHY2251 was related to the activation of the caspase cascade, which was significantly attenuated by pre-treatment with Z-VAD-FMK, a pan-caspase inhibitor. Furthermore, MHY2251 stimulated the phosphorylation of c-Jun N-terminal kinase (JNK), and MHY2251-triggered apoptosis was blocked by pre-treatment with SP600125, a JNK inhibitor. This finding indicated the specific involvement of JNK in MHY2251-induced apoptosis. MHY2251 shows considerable potential as a therapeutic agent for targeting human CRC via the inhibition of SIRT1 and activation of JNK/p53 pathway.

• Journal of the Korean Society of Food Culture
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• v.23 no.3
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• pp.318-327
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• 2008

This study examined the cultural dietary habits as well as attitudes toward food, within other life pattern elements, of students living in Gwangju City and Chonnam Province, Korea. Questionnaires from 1,000 student respondents were analyzed. The survey consisted of questions regarding physical condition and health status, dietary consciousness, food preference, knowledge of food and nutrition, and dietary culture. The results showed that 1.6% of the students considered their own physical condition to be extremely poor, and 2.7% and 2.1% also considered their father's and mother's physical conditions as extremely poor, respectively. Among the respondents, 18.3% were smokers and consumed an average of 14.8 cigarettes per day. With regard to their dietary habits, the students answered that they preferred to eat meals with friends rather than with family members, fruit was chosen for eating over health food supplements, and there was very little participation or interest in various food and cultural festivals. The female students had a tendency to alleviate mental stresses by eating, while the male students performed more physical activity to deal with stress. The female students also preferred cereal, fruit, fast food, and sweetened foods more than the male students. Between the smokers and non-smokers, significantly more non-smokers chose fruit (p<0.01), ethnic foods (p<0.05), and sweetened foods (p<0.05) as compared to the smokers. Body mass index (BMI) had significant positive correlations with soft drink (p<0.01), health food supplement (p<0.01), and alcoholic beverage (p<0.001) consumption, while BMI was negatively correlated with cereal (p<0.01), fruit (p<0.001), and sweetened food (p<0.01) intake. The health status of students was positively correlated with their father's health status (p<0.01), mother's health status (p<0.001), and BMI (p<0.05), as well as cereal (p<0.001), high protein side dish (p<0.01), fruit (p<0.01), vegetable (p<0.01), and traditional food (p<0.001) intake. The average body weight for female students was approximately 5 kg less than the Korean Nutrition Society's standardized weight, therefore, it is strongly recommended that measures be taken to develop a systematic nutrition education program that would help those students who often unintentionally skip breakfast or go on extreme diets to improve body image.

• Journal of Life Science
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• v.34 no.1
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• pp.9-17
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• 2024

Diabetes mellitus (DM) is one of the main global health problems. Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, a process that is termed glucose toxicity. Our perspective about glucose toxicity as it pertains to the pancreatic β-cell is that the characteristic decreases in insulin secretion are caused by regulated apoptotic gene expression. In this study, we examined whether ferulic acid protects INS-1 pancreatic cells against high glucose-induced apoptosis. High glucose concentration (30 mM) induced glucotoxicity and death of INS-1 pancreatic β cells. However, treatment with 1, 5, 10, or 20 μM ferulic acid increased the cell viability in a concentration-dependent manner. Treatment with ferulic acid dose-dependently decreased the intracellular levels of reactive oxygen species, thiobarbituric acid reactive substances, and nitric oxide in INS-1 pancreatic β cells pretreated with high glucose. These effects influence the apoptotic pathway, increasing the expression of the anti-apoptotic protein Bcl-2 and reducing the levels of pro-apoptotic proteins, including Bax, cytochrome C, and caspase 9. Annexin V/propidium iodide staining indicated that ferulic acid significantly reduced high glucose-induced apoptosis. These results demonstrate that ferulic acid is a potential therapeutic agent to protect INS-1 pancreatic β cells against high glucose-induced apoptosis.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.154-161
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• 2024

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder that causes progressive paralysis. L-Citrulline is a nonessential neutral amino acid produced by L-arginine via nitric oxide synthase (NOS). According to previous studies, the pathogenesis of ALS entails glutamate toxicity, oxidative stress, protein misfolding, and neurofilament disruption. In addition, L-citrulline prevents neuronal cell death in brain ischemia; therefore, we investigated the change in the transport of L-citrulline under various pathological conditions in a cell line model of ALS. We examined the uptake of [¹⁴C]L-citrulline in wild-type (hSOD1wt/WT) and mutant NSC-34/ SOD1^G93A (MT) cell lines. The cell viability was determined via MTT assay. A transport study was performed to determine the uptake of [¹⁴C]L-citrulline. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was performed to determine the expression levels of rat large neutral amino acid transported 1 (rLAT1) in ALS cell lines. Nitric oxide (NO) assay was performed using Griess reagent. L-Citrulline had a restorative effect on glutamate induced cell death, and increased [¹⁴C]L-citrulline uptake and mRNA levels of the large neutral amino acid transporter (LAT1) in the glutamate-treated ALS disease model (MT). NO levels increased significantly when MT cells were pretreated with glutamate for 24 h and restored by co-treatment with L-citrulline. Co-treatment of MT cells with L-arginine, an NO donor, increased NO levels. NSC-34 cells exposed to high glucose conditions showed a significant increase in [¹⁴C]L-citrulline uptake and LAT1 mRNA expression levels, which were restored to normal levels upon co-treatment with unlabeled L-citrulline. In contrast, exposure of the MT cell line to tumor necrosis factor alpha, lipopolysaccharides, and hypertonic condition decreased the uptake significantly which was restored to the normal level by co-treating with unlabeled L-citrulline. L-Citrulline can restore NO levels and cellular uptake in ALS-affected cells with glutamate cytotoxicity, pro-inflammatory cytokines, or other pathological states, suggesting that L-citrulline supplementation in ALS may play a key role in providing neuroprotection.

• Journal of Korean Neurosurgical Society
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• v.67 no.5
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• pp.510-520
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• 2024

Objective : Parkinson's disease (PD) is one of the most prevalent neurodegenerative diseases, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. The treatment of PD aims to alleviate motor symptoms by replacing the reduced endogenous dopamine. Currently, there are no disease-modifying agents for the treatment of PD. Zebrafish (Danio rerio) have emerged as an effective tool for new drug discovery and screening in the age of translational research. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is known to cause a similar loss of dopaminergic neurons in the human midbrain, with corresponding Parkinsonian symptoms. L-type calcium channels (LTCCs) have been implicated in the generation of mitochondrial oxidative stress, which underlies the pathogenesis of PD. Therefore, we investigated the neuro-restorative effect of LTCC inhibition in an MPTP-induced zebrafish PD model and suggested a possible drug candidate that might modify the progression of PD. Methods : All experiments were conducted using a line of transgenic zebrafish, Tg(dat:EGFP), in which green fluorescent protein (GFP) is expressed in dopaminergic neurons. The experimental groups were exposed to 500 μmol MPTP from 1 to 3 days post fertilization (dpf). The drug candidates : levodopa 1 mmol, nifedipine 10 μmol, nimodipine 3.5 μmol, diethylstilbestrol 0.3 μmol, luteolin 100 μmol, and calcitriol 0.25 μmol were exposed from 3 to 5 dpf. Locomotor activity was assessed by automated tracking and dopaminergic neurons were visualized in vivo by confocal microscopy. Results : Levodopa, nimodipine, diethylstilbestrol, and calcitriol had significant positive effects on the restoration of motor behavior, which was damaged by MPTP. Nimodipine and calcitriol have significant positive effects on the restoration of dopaminergic neurons, which were reduced by MPTP. Through locomotor analysis and dopaminergic neuron quantification, we identified the neuro-restorative effects of nimodipine and calcitriol in zebrafish MPTP-induced PD model. Conclusion : The present study identified the neuro-restorative effects of nimodipine and calcitriol in an MPTP-induced zebrafish model of PD. They restored dopaminergic neurons which were damaged due to the effects of MPTP and normalized the locomotor activity. LTCCs have potential pathological roles in neurodevelopmental and neurodegenerative disorders. Zebrafish are highly amenable to high-throughput drug screening and might, therefore, be a useful tool to work towards the identification of disease-modifying treatment for PD. Further studies including zebrafish genetic models to elucidate the mechanism of action of the disease-modifying candidate by investigating Ca2+ influx and mitochondrial function in dopaminergic neurons, are needed to reveal the pathogenesis of PD and develop disease-modifying treatments for PD.

• Journal of Animal Science and Technology
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• v.51 no.3
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• pp.207-216
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• 2009

This experiment was conducted to investigate the effects of dietary supplementation of organic acid mixture on growth performance, cecal microflora, blood characteristics and immune response in broiler chicks and to prove the possibility of organic acid mixture as an alternative to antibiotics growth promotor. A total of four hundred eighty, 1-day-old male broiler chicks (Ross$\times$Ross 308) were randomly divided into 4 groups with 4 replicates of 30 birds each. The treatments were NC (free antibiotics), PC (basal diet with virginiamycin 10 ppm and salinomycin 60 ppm), 0.3% organic acid, and 0.5% organic acid. The final body weight and body weight gain were significantly higher in organic acid 0.5% than NC (P<0.05). The feed conversion ratio in all treated groups were significantly improved as compared to that of NC (P<0.05). The carcass rate and relative organs weight were not significantly difference among the groups. The relative weight and length of small intestine in PC were significantly decreased than the other groups. The numbers of cecal coliform bacteria and Salmonella in all treated groups were significantly lower than NC (P<0.05). The number of cecal lactic acid bacteria was not different among the groups. No significant differences among the groups were observed in the contents of total cholesterol, triglyceride, blood urea nitrogen (BUN), albumin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) in blood serum. The contents of total protein and globulin in blood serum of PC and organic acid treated groups were significantly increased as compared to those of NC (P<0.05). Therefore, albumin:globulin ratio of PC and organic acid treated groups was significantly lower than NC (P<0.05). The total white blood cell (WBC), heterophil, lymphocyte, and stress indicator (heterophil:lymphocyte ratio) were not significantly different among the groups. No significant difference was observed on the expression rate of splenic cytokines mRNA in organic acid treated groups compared to the control. Consequently, supplemental organic acid mixture improved the growth performance, and influenced positive effects on the intestinal microflora by inhibiting the growth of harmful bacteria without any adverse effects on relative weights of organs and blood biochemical parameters in broiler chicks.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.17 no.12
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• pp.407-414
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• 2016

This study was conducted to investigate the effects of supplementation of dietary betaine on nutrient digestibility and physiological responses in finishing pigs. A total of twelve pigs with a body weight of $80.1{\pm}3.7kg$ were individually caged, and randomly assigned to one of the two experimental diets containing 0 (control) or 5 g/kg (treatment) of the betaine in a $2{\times}2$ Latin square design. The experimental period was 14 days-7 days adaptation and 7 days trial period-per phase. All data for the difference between control and treatment groups were statistically analyzed by student's t-test. Dry matter and crude protein digestibility in the treatment group were significantly improved by 1% and 1.3%, respectively, as compared with those in the control (p<0.05). The apparent absorption of dietary energy was increased from 82.3% to 83.7% by dietary betaine supplementation. Thus, the retention of energy was also significantly increased to above 6% in the treatment group compared with the control group (control 4,057 vs treatment 4,314 kcal; p<0.01). The physiological parameters indicating serum biochemical contents and stress-, immune-, and inflammatory- responses were not changed by the supplementation of dietary betaine. In conclusion, dietary betaine improves the nutrient digestibility without any negative effects in terms of physiology in finishing pigs. It suggests that the supplementation of dietary betaine may increase the productivity through the improvement of weight gain and feeding efficiency.

• Tuberculosis and Respiratory Diseases
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• v.69 no.1
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• pp.16-23
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• 2010

Background: Most lung cancer patients receive systemic chemotherapy at an advanced stage disease. Cisplatin-based chemotherapy is the main regimen for treating advanced lung cancer. Recently, autophagy has become an important mechanism of cellular adaptation under starvation or cell oxidative stress. The purpose of this study was to determine whether or not autophagy can occurred in cisplatin-treated lung cancer cells. Methods: H460 cells were incubated with RPMI 1640 and treated in $5{\mu}M$ or $20{\mu}M$ cisplatin concentrations at specific time intervals. Cells surviving cisplatin treatment were measured and compared using an MTT cell viability assay to cells that underwent apoptosis with autophagy by nuclear staining, apoptotic or autophagic related proteins, and autophagic vacuoles. The development of acidic vascular organelles was using acridine orange staining and fluorescent expression of GFP-LC3 protein in its transfected cells was observed to evaluate autophagy. Results: Lung cancer cells treated with $5{\mu}M$ cisplatin-treated were less sensitive to cell death than $20{\mu}M$ cisplatin-treated cells in a time-dependent manner. Nuclear fragmentation at $5{\mu}M$ was not detected, even though it was discovered at $20{\mu}M$. Poly (ADP-ribose) polymerase cleavages were not detected in $5{\mu}M$ within 24 hours. Massive vacuolization in the cytoplasm of $5{\mu}M$ treated cells were observed. Acridine orange stain-positive cells was increased according in time-dependence manner. The autophagosome-incorporated LC3 II protein expression was increased in $5{\mu}M$ treated cells, but was not detected in $20{\mu}M$ treated cells. The expression of GFP-LC3 were increased in $5{\mu}M$ treated cells in a time-dependent manner. Conclusion: The induction of autophagy occurred in $5{\mu}M$ dose of cisplatin-treated lung cancer cells.