• Journal of the Korean Chemical Society
• /
• v.50 no.3
• /
• pp.216-223
• /
• 2006

To increase the stability of liposomes in blood circulation, surface modification of liposomes by incorporating a lipid-polymer derivative in the lipid bilayer or conjugating a hydrophilic polymer to the liposomal surface has been developed. In this study, the comblike copolymer, poly(HEMA-co-HPOEM), having multiple polyethyleneoxide side chains was prepared by free radical polymerization of hydroxyethylmethacrylate (HEMA) and hydroxypolyoxyethylenemethacrylate (HPOEM) as vinyl monomers. Poly(HEMA-co-HPOEM) was conjugated to the liposomal surface and the characteristics of the modified liposomes in serum were investigated. Conjugation of poly(HEMA-co-HPOEM) to liposomes increased the particle size of the liposomes by 30 nm and decreased the absolute value of zeta potential of the liposomes by shielding the negative charge of liposomal surface. Loading efficiency of model drug, doxorubicin, in liposomes was about 90% and the efficiency was not affected by conjugation of poly(HEMA-co-HPOEM) to liposomes. The particle size of poly(HEMA-co-HPOEM)-conjugated liposomes in serum did not changed and the protein adsorption was lower than that of control liposomes or liposomes containing polyethyleneoxide-lipid derivative (PEG-liposomes). These results suggest that poly(HEMA-co-HPOEM) is efficient for the stabilization of liposomes in blood circulation.

• Journal of Food Hygiene and Safety
• /
• v.34 no.3
• /
• pp.303-308
• /
• 2019

L-carnitine is found in high levels in muscle tissues. It has been developed as a nutrient and dietary supplement, and also used as a therapeutic supplement in various diseases including type II diabetes, osteoporosis and metabolic neuropathies. However, it is not fully understood how it affects cellular mechanisms in colorectal cancer. Therefore, we attempted to determine the effect of L-carnitine in HCT116 human colorectal cancer cells. First, the HCT116 cells were exposed to L-carnitine for 24 hours at 0-40 mM, and then analyzed for cellular proliferation, oxidative stress and related mechanisms. In a MTT assay, L-carnitine inhibited cellular proliferation and induced reactive oxygen species (ROS) in HCT116 by DCF-DA analysis. To analyze the mechanism of L-carnitine in colorectal cancer cells, we performed a western blot analysis for pERK1/2 and pp38 MAP kinase. The western blot showed that L-carnitine significantly increased protein levels of pERK1/2 and pp38 compared with control. Taken together, we found that L-carnitine has anti-proliferative function via increased ROS and activation of ERK1/2 and p38 pathway in HCT116. These findings suggest that L-carnitine may have an anti-proliferative role on colorectal cancer.

• Journal of Life Science
• /
• v.30 no.12
• /
• pp.1070-1077
• /
• 2020

Treatment with anticancer drugs changes the expression of multiple genes related to cell proliferation, migration, and drug resistance. These changes in gene expression may be connected to regulatory networks for each other. This study showed that doxorubicin treatment induces the expression of oncogenic FosB and decreases the expression of oncogenic SETDB1 in A549 and H1299 human lung cancer cells, which are different in tumor suppressor p53 status. However, a small difference was detected in the quantitative expression of those proteins in the two kinds of cells. To examine the potential regulation of SETDB1 and FosB by p53, we predicted putative p53 binding sites on the genomic DNA of SETDB1 and FosB using a TF motif binding search program. These putative p53 binding sites were identified as 18 sites in the promoter regions of SETDB1 and 21 sites in the genomic DNA of FosB. A luciferase assay confirmed that p53 negatively regulated the promoter activities of SETDB1 and FosB. Furthermore, the results of RT-PCR, western blot, qPCR, and immunostaining experiments indicated that the transfection of exogenous p53 decreases the expression of SETDB1 and FosB in H1299 cells. This indicates that p53 negatively regulates the expression of SETDB1 and FosB at the transcriptional level. Collectively, the downregulation of SETDB1 and FosB by p53 may provide functional networks for apoptosis and for the survival of cancer cells during anticancer drug treatment.

• Clean Technology
• /
• v.27 no.1
• /
• pp.55-60
• /
• 2021

Antibiotics are compounds broadly used to treat patients with infectious diseases and to enhance productivity in agriculture, fisheries, and livestock industries. However, due to the overuse of antibiotics and their low biodegradability, a substantial amount of antibiotics is leaking into the sewer, subsequently resulting in pollution and the emergence of antibiotic-resistant bacteria. This study explores biodegradable serum albumin's potential as an adsorbent to remove antibiotics from water. Serum albumin is a natural blood protein that transports various metabolites and hormones to all tissues' extravascular spaces. While serum albumin is highly water-soluble, it has intrinsic binding sites which readily accommodate ionic, hydrophilic, or hydrophobic molecules, rendering it a good building block for a nano-adsorbent. To induce coacervation, a desolvating agent, ethanol, was added dropwise into the aqueous albumin solution, resulting in dehydration and liquid-liquid phase separation of albumins into albumin nanoparticles within a size range of 150 ~ 170 nm. The addition of glutaraldehyde as a cross-linker improved the size stability and homogeneity of albumin nanoparticles. Adsorption of amoxicillin antibiotics on albumin nanoparticles was dependent upon glutaraldehyde concentration used in desolvation and pH during adsorption. The maximum adsorption capacity measured by spectrophotometry was found to be 12.4 micrograms of amoxicillin per milligram of albumin nanoparticle. These results demonstrate serum albumin's potential as a building block for fabricating a natural nano-adsorbent to remove antibiotics from water.

• Korean Journal of Food Science and Technology
• /
• v.54 no.3
• /
• pp.288-296
• /
• 2022

This study aimed to verify the effect of Citrus unshiu peel water extract (CUP) on a mouse model of acute gastritis (AG) induced by HCl/ethanol. Several studies have found that CUP has anti-inflammatory effects. The AG model was induced by oral administration of 150 mM HCl/60% ethanol (550 µL) to all groups except the control group. Also, for drug treatment, sucralfate (10 mg/kg) and CUP (100 or 200 mg/kg) were orally administered for 90 minutes before induction. The effect of CUP treatment was confirmed by gross gastric mucosal damage measurement, and the levels of Glutamic Oxaloacetic Transaminase (GOT), Glutamic Pyruvic Transaminase (GPT), and myeloperoxidase were reduced as well as the levels of oxidative stress biomarkers and their related proteins. In addition, the levels of inflammatory proteins, mediators, and cytokines were significantly downregulated byPI3K/Akt signaling. Taken together, these results show that CUP treatment alleviates AG by regulating PI3K/Akt signaling.

• Korean Journal of Psychosomatic Medicine
• /
• v.32 no.1
• /
• pp.1-9
• /
• 2024

Frailty is a clinical syndrome as an increased vulnerability to stressors, leading to a decrease in physiologic reserves and a decline in the ability to maintain a good homeostasis. This condition leads to an increased risk of hospitalization, disability and mortality. Frailty occurs due to various causes and requires a multidimensional approach. It is also important to detect and manage it early. Frailty is also deeply related to neuropsychiatric problems such as pain and depression. In evaluating frailty, it is desirable to comprehensively consider not only physical areas such as disease, nutrition, movement, and sensory functions, but also psychosocial areas, and representative scales include Fried's physical frailty phenotype and Rockwood's frailty index. Physical activity and appropriate protein intake are important for frailty management, and inappropriate drug use should be reduced and oral care, cognitive function, and falls should also be noted. Frailty and pain can affect each other, and pain can promote frailty. Evidence has been published that hormone and protein abnormalities, immune system activity and inflammatory response, and epigenetic mechanisms work in common in the field of frailty and pain. More extensive and high-quality research should be conducted in the future, and the quality of life will be improved if the results are applied to the suppression and treatment of old age and pain.

• Journal of Korean society of Dental Hygiene
• /
• v.24 no.3
• /
• pp.219-227
• /
• 2024

Objectives: The pulp is the center of the tooth containing nerves and blood vessels. The condition in which the pulp becomes inflamed due to caries or periodontitis is called pulpitis. Pulpitis is a difficult-to-treat disease and causes peripheral nerve tissue changes and severe pain; however, the relationship between neuronal activity and voltage-gated sodium channel 1.7 (Nav1.7) expression in the trigeminal ganglion (TG) during pulpitis has not been well studied. In this study, we found that experimentally induced pulpitis activates Nav1.7 expression in the periphery, leading to neuronal overexpression in the TG. Thus, we sought to identify ways to regulate this process. Methods: Acute pulpitis was induced in rat maxillary molars by treating the pulp with allyl isothiocyanate (AITC). Three days later, in vivo optical imaging was used to record and compare neural activities in the TG. Western blotting was used to identify molecular changes in terms of the expression of extracellular signal-regulated kinase (ERK), c-Fos, transient receptor potential ankyrin 1 (TRPA1), and collapsin response mediator protein-2 (CRMP2) in the brain stem. Results: The results confirmed the neurological changes in the TGs of the pulpitis model, and histological and molecular biological evidence confirmed that increased Nav1.7 expression induced by pulpitis leads to pain. Furthermore, selective inhibition of Nav1.7 resulted in changes in neural activity, suggesting that pulpitis induces increased Nav1.7 expression, and that effective control of Nav1.7 could potentially reduce pain. Conclusions: The inhibition of overexpressed Nav1.7 channels may modulate nociceptive signal processing in the brain and effectively control pain associated with pulpitis.

• Food Science and Preservation
• /
• v.23 no.3
• /
• pp.378-386
• /
• 2016

Anti-atherogenic effects in tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-stimulated human umbilical vein endothelial cells (HUVEC) are involved in the suppression of oxidative stress, cell adhesion molecules, and pro-inflammatory factors. This study investigated the vascular inflammation inhibitory activity of traditional Doenjang plays a key role in the pathogenesis and progression of atherosclerosis. The protective effects of Korean Deonjang was investigated on the expression of cell adhesion molecules (CAMs) in tumor necrosis factor (TNF)-${\alpha}$-induced human umbilical vascular endothelial cells (HUVECs). Deonjang extracts (20, 50, $100{\mu}g/mL$) decreased the expression of 20 ng/mL TNF-${\alpha}$-induced vascular cell adhesion molecule (VCAM)-1 intracellular adhesion molecule (ICAM)-1 proteins, and their corresponding mRNA levels. Nitric oxides (NO) produced by endothlial nitric oxides synthase (eNOS) dilated blood vessels, which had protective effects against platelet and leukocyte adhesion. While TNF-${\alpha}$-induced suppressed the production of nitric oxide in HUVECs, Doenjang restored NO production in HUVECs. In addition, Deonjang reduced the TNF-${\alpha}$-induced expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 mRNA levels. These results suggested that Doenjang can inhibited the production of cell adhesion molecules and inflammatory mediators, which could be a potential candidate for preventing atherosclerosis.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.41 no.9
• /
• pp.1205-1210
• /
• 2012

This study investigated the anti-inflammatory effects of Ligustrum ovalifolium H. (LOH) leaf extracts on RAW264.7 macrophages. Cell toxicity was determined by MTT assay. We evaluated the anti-inflammatory effects of LOH extracts by measuring nitric oxide (NO), reactive oxygen species (ROS), inducible NOS (iNOS) production, and cyclooxygenase-2 (COX-2) expression by Western blotting. LOH ethanolic extracts (0.05, 0.1, and 0.2 mg/mL) significantly suppressed LPS-stimulated production of NO. The intracellular ROS level also significantly decreased. LOH ethanolic extracts reduced the expression of iNOS and COX-2 proteins. The present results show that LOH ethanol extract has potent anti-inflammatory effects on RAW264.7 macrophages. These results also suggest that the anti-inflammatory effects of LOH extracts may be related to the inhibition of LPS-stimulated ROS and NO production. Therefore, ethanolic extracts of LOH leaves may be utilized as a good source of functional foods for protection against inflammatory diseases.

• Journal of Life Science
• /
• v.18 no.6
• /
• pp.796-803
• /
• 2008

Mutations in the APP gene lead to enhanced cleavage by ${\beta}-$ and ${\gamma}-secretase$, and increased $A{\beta}$ formation, which are closely associated with Alzheimer's disease (AD)-like neuropathological changes. Recent studies have shown that exercise training can ameliorate pathogenic phenotypes ($A{\beta}-42$, BDNF, GLUT-1 and HSP70) in experimental models of Alzheimer's disease. Here, we have used NSE/APPsw transgenic mice to investigate directly whether exercise training ameliorates pathogenic phenotypes within Alzheimer's brains. Sixteen weeks of exercise training resulted in a reduction of $A{\beta}-42$ peptides and also facilitated improvement of cognitive function. Furthermore, GLUT -1 and BDNF proteins produced by exercise training may protect brain neurons by inducing the concomitant expression of genes that encode proteins (HSP-70) which suppress stress induced neuron cell damages from APPsw transgenic mice. Thus, the improved cognitive function by exercise training may be mechanistically linked to a reduction of $A{\beta}-42$ peptides, possibly via activation of BDNF, GLUT-1, and HSP-70 proteins. On the basis of the evidences presented in this study, exercise training may represent a practical therapeutic management strategy for human subjects suffering from Alzheimer's disease.