• Proceedings of the PSK Conference
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• 2002.10a
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• pp.249.1-249.1
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• 2002

This study was carried out to demonstrate the effects of oral administration of DA-8159. a selective phosphodiesterase 5 inhibitor. on development of pulmonary hypertension induced by monocrotaline (MCT). MCT-treated rats(60mg/kg) were divided into three groups and orally administered vehicle, 1 mg/kg or 5 mg/kgg of DA-8159 twice a day for 3 weeks. Increased right ventricular weights, medial wall thickening in pulmonary arteries. myocardial fibrosis, decrease of plasma cyclic guanosine monophosphate (cGMP) level and body weight gains were shown in MCT group. (omitted)

• Biomolecules & Therapeutics
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• v.21 no.1
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• pp.42-48
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• 2013

Nystatin, a polyene antifungal antibiotic, is a cholesterol sequestering agent. The antifungal agent alters composition of the plasma membrane of eukaryotic cells, whereas its effects on cells are poorly investigated. In the current study, we investigated the question of whether nystatin was able to induce expression of macrophage inflammatory protein-1 (MIP-1). THP-1 cells rarely express MIP-$1{\alpha}$ and MIP-$1{\beta}$, however, upon exposure to nystatin, significantly elevated expression of MIP-$1{\alpha}$ and MIP-$1{\beta}$ was observed in a dose-dependent fashion at the messenger and protein levels. Cellular factors activated by nystatin as well as involved in nystatin-induced expression of MIP-1 proteins were identified in order to understand the molecular mechanisms of action of the anti-fungal agent. Treatment with nystatin resulted in enhanced phosphorylation of Akt, ERK, p38 MAPK, and JNK. Abrogation or significant attenuation of nystatin-induced expression of MIP-$1{\alpha}$ and MIP-$1{\beta}$ was observed by treatment with Akt inhibitor IV, LY294002, and SP6001250. Inhibition of ERK or p38MAPK using U0126 and SB202190 did not lead to attenuation of MIP-1 expression. In addition, inhibitors of protein kinase C, such as GF109203X and Ro-318220, also attenuated expression of MIP-1. These results indicate that nystatin is able to activate multiple cellular kinases and, among them, Akt and JNK play primary roles in nystatin-induced expression of MIP-1 proteins.

• Journal of the Korean Applied Science and Technology
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• v.35 no.4
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• pp.1369-1378
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• 2018

The purpose of this study was to investigate the effect of skate skin collagen peptide (SCP) according to its molecular weight (<1,000 Da or >1,000 Da) which was divided using the ultrafilatration method. The 200 mg/kg collagen peptide was administrated to obesity-induced db/db mice for 8 weeks. As the results, in collagen peptide-treated groups, body weight gain was decreased, the plasma and hepatic concentration of reactive oxygen species decreased and oxidative stress was alleviated. In addition, SCP-treated group showed the significant reduction of the protein expressions of nuclear transcription factors($NF-{\kappa}B$), enzymes(COX2, iNOS), and inflammatory cytokine(IL-6) in hepatic tissue, compared with those of the obese control group. There was a slight difference depending on the molecular weight of collagen peptide, but overall it was not significant. Therefore, SCP effectively inhibited the obesity-induced inflammatory response through attenuation of oxidative stress in the liver.

• The Bulletin of The Korean Astronomical Society
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• v.46 no.2
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• pp.47.3-48
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• 2021

We studied the large scale dynamo process in a system forced by helical magnetic field. The dynamo process is basically nonlinear, but can be linearized with 𝛼&𝛽 coefficients and large scale magnetic field $\bar{B}$. This is very useful to the investigation of solar (stellar) dynamo. A coupled semi-analytic equations based on statistical mechanics are used to investigate the exact evolution of 𝛼&𝛽. This equation set needs only magnetic helicity ${\bar{H}}_M({\equiv}{\langle}{\bar{A}}{\cdot}{\bar{B}}{\rangle},\;{\bar{B}}={\nabla}{\times}{\bar{A}})$ and magnetic energy ${\bar{E}}_M({\equiv}{\langle}{\bar{B}}^2{\rangle}/2)$. They are fundamental physics quantities that can be obtained from the dynamo simulation or observation without any artificial modification or assumption. 𝛼 effect is thought to be related to magnetic field amplification. However, in reality the averaged 𝛼 effect decreases very quickly without a significant contribution to ${\bar{B}}$ field amplification. Conversely, 𝛽 effect contributing to the magnetic diffusion maintains a negative value, which plays a key role in the amplification with Laplacian ∇²(= - k²) for the large scale regime. In addition, negative magnetic diffusion accounts for the attenuation of plasma kinetic energy E_V(= 〈 U² 〉/2) (U: plasma velocity) when the system is saturated. The negative magnetic diffusion is from the interaction of advective term - U • ∇ B from magnetic induction equation and the helical velocity field. In more detail, when 'U' is divided into the poloidal component U_pol and toroidal one U_tor in the absence of reflection symmetry, they interact with - B • ∇ U and - U • ∇ B from ∇ × 〈 U × B 〉 leading to 𝛼 effect and (negative) 𝛽 effect, respectively. We discussed this process using the theoretical method and intuitive field structure model supported by the simulation result.

• Journal of Microbiology and Biotechnology
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• v.30 no.3
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• pp.382-390
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• 2020

Periplanetasin-4 is an antimicrobial peptide with 13 amino acids identified in cockroaches. It has been reported to induce fungal cell death by apoptosis and membrane-targeted action. Analogs were designed by substituting arginine residues to modify the electrostatic and hydrophobic interactions accordingly and explore the effect of periplanetasin-4 through the increase of net charge and the decrease of hydrophobicity. The analogs showed lower activity than periplanetasin-4 against gram-positive and gram-negative bacteria. Similar to periplanetasin-4, the analogs exhibited slight hemolytic activity against human erythrocytes. Membrane studies, including determination of changes in membrane potential and permeability, and fluidity assays, revealed that the analogs disrupt less membrane integrity compared to periplanetasin-4. Likewise, when the analogs were treated to the artificial membrane model, the passage of molecules bigger than FD4 was difficult. In conclusion, arginine substitution could not maintain the membrane disruption ability of periplanetasin-4. The results indicated that the attenuation of hydrophobic interactions with the plasma membrane caused a reduction in the accumulation of the analogs on the membrane before the formation of electrostatic interactions. Our findings will assist in the further development of antimicrobial peptides for clinical use.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.4
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• pp.323-331
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• 2001

A splanchic artery occlusion for 90 min followed by reperfusion of the mesenteric circulation resulted in a severe form of circulatory shock characterized by endothelial dysfunction, severe hypotension, marked intestinal tissue injury, and a high mortality rate. The effect of rutin, a flavonoid having antiprostanoid, anti-inflammatory, antithrombotic, antioxidant effect, were investigated in a model of splanchnic artery occlusion (SAO) shock in urethane anesthetized rats. Occlusion of the superior mesenteric artery for 90 min produced a severe shock state resulted in a fatal outcome within 120 min of reperfusion in many rats. Rutin was given as a bolus (1.28 mg/kg) 10 min prior to reperfusion. Administration of rutin significantly improved mean arterial blood pressure in comparison to vehicle treated rats (p＜0.05). Rutin treatment also resulted in a significant attenuation in the increase in plasma amino nitrogen concentration, intestinal myeloperoxidase activity, intestinal lipid peroxidation, infiltration of neutrophils in intestine and thrombin induced adherence of neutrophils to superior mesentric artery segments. These results suggest that rutin provides beneficial effects in part by preserving endothelial function and attenuating neutrophil accumulation in the ischemic reperfused splanchnic circulation.

• Nutritional Sciences
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• v.6 no.1
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• pp.20-24
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• 2003

The effect of a-tocopherol on the formation and accumulation of phospholipid hydroperoxides, especially of phosphatidylcholine hydroperoxides, in the tissues of 2, 2 -azobis Hydrochloride (AAPH) - dosed rats was investigated. In a-tocopherol supplemented rats, the activities of glutathione peroxidase, catalase and superoxide dismutase were significantly inhibited, compared with the AAPH group. AAPH treatment led to oxidation of phospholipids in the liver, lungs, brain, plasma and red blood cells (RBC), resulting in a notable increase in phosphatidylcholine hydroperoxide (PCOOH). All tissues of the rats given an $\alpha$-tocopherol supplement showed an attenuation of the stimulating effect of AAPH, leading to low levels of formation of PCOOH. Also, the rats injected with AAPH and a-tocopherol showed relatively normal-appearing hepatocytes, except for a little loss of the granules. With regards to the morphological appearance of the liver, it was observed that oral intakes of a -tocopherol resulted in an antioxidant defense against attacks of peroxyl radicals. Thus, we suggest that a-tocopherol is potentially helpful in protecting membrane phospholipids against oxidative damage in vivo.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.579-586
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• 1999

Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement- dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg) to I/R hearts in the presence of PMNs $(100{\times}10^6)$ and homologous plasma improved coronary flow and preserved cardiac contractile function (p＜0.001) in comparison to those I/R hearts receiving only vehicle. In addition, C1 INH significantly (p＜0.001) reduced PMN accumulation in the ischemic myocardium as evidenced by an attenuation in myeloperoxidase activity. These findings demonstrate the C1 INH is a potent and effective cardioprotective agent inhibits leukocyte-endothelial interaction and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.

• Food Science and Biotechnology
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• v.16 no.6
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• pp.988-993
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• 2007

The protective effect of the water extract of Fraxinus rhynchophylla leaves (FLE) was determined using an animal model of acetaminophen (AAP)-induced nephrotoxicity. The BALB/c male mice used in this study were divided into 3 groups; the normal, AAP-administered, and FLE-pretreated AAP groups. A single dose of AAP induced necrosis of renal tubules and congestion along with edema to a remarkable degree as observed by hematoxylin and eosin stain, and also increased the numbers of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL)-positive renal tubular epithelial cells. Blood urea nitrogen and plasma creatinine levels were determined to be significantly higher in the AAP group than in the normal group. However, FLE pretreatment resulted in an attenuation of renal tubule necrosis. Regeneration and dilatation of renal tubules were noted, and the numbers of TUNEL-positive cells were reduced in the FLE-pretreated groups. In an effort to detect the bioactive compounds exerting protective effects in FLE, the analysis of phenolic compounds via gas chromatography/mass spectrometry (GC/MS) were performed, and identified esculetin and esculin. The present study indicates that these compounds may exert a protective effect against AAP-induced nephrotoxicity.

• Journal of Veterinary Clinics
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• v.36 no.3
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• pp.145-149
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• 2019

Previous report has suggested that the albumin levels were reduced in the peripheral blood mononuclear cells (PBMCs) and consequently oxidative stress was elevated in streptozotocin (STZ)-induced diabetic rats as albumin is the predominant antioxidant in plasma. In this study, we suggest that the levels of pro-inflammatory cytokine such as interleukin-6 (IL-6) and tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$) were increased by approximately 3.4- and 2.9-fold, respectively, in the serum of STZ-diabetic rats, compared to those of normal rat. In addition to the cytokines, the levels of C-reactive protein (CRP) were also about 3.6-fold higher, indicating that STZ induced a pro-inflammatory response in rat blood. However, when purified rat albumin was externally co-administrated with STZ through the tail vein, the serum levels of IL-6, $TNF-{\alpha}$, and CRP were markedly reduced, although the values were still higher than those of normal (non-diabetic) rats. Albumin administration also decreased STZ-induced oxidative stress in serum and PBMCs. Moreover, the decrease in cytokine and CRP levels was dependent on the dose of injected albumin. These results suggest that STZ-induced pro-inflammation and oxidative stress in rat blood might be attenuated by treatment with exogenous albumin.