• Korean Journal of Pharmacognosy
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• v.47 no.2
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• pp.137-142
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• 2016

Enterovirus is a common cause of several severe diseases such as myocarditis, hand-foot-mouth disease, and meningitis in children and adult. There are many try to develop new antiviral drug for direct treatment in virus infection. However, synthetic chemical antiviral drug is not working. To overcome this limitation, we examined plant extracts. The antiviral effect of plant extracts was screened by HeLa cell survival assay in coxsackievirus B3 (CVB3) infection. We observed a strong antiviral effect of Poria cocos extract in a dose-dependent manner (1 mg/ml~0.01 mg/ml). P. cocos extract (1 mg/ml) treatment was dramatically decreased virus protease 2A induced eIF4G-I cleavage and virus capsid protein VP1 production. CVB3 positive and negative strand RNA amplification were significantly reduced in P. cocos extract treatment. P. cocos extract completely blocked early time activation of ERK and AKT activity in CVB3 infection. Taken together these data indicate that the treatment of P. cocos extract strongly inhibit CVB3 replication. Poria cocos extract may possible to developed as a therapeutic agent for enterovirus.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1305-1308
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• 2003

To evaluate the neurotoxicity of reactive oxygen species (ROS) in cultured cultured spinal dorsal root(DRG) neurons derived from neonatal mouse, Cytotoxicity was measured by MTS assay after cultured cells were grown for 3 hours in the media containing 1～60 μM hydrogen peroxide (H₂O₂). In addition the neuroprotective effect of Salviae Miltiorrhzae Radix (SMR) was measured in these cultrures. Cell viability was positively decreased in a dose- and time-dependent manner after exposure of cultured mouse DRG neurons to 30 tt M H202 for 3 hours. In the neuroprotective effect of SMR on H₂O₂-mediated toxicity, SMR prevented the H₂O₂-induced neurotoxicity in these cultures. From these results. it suggests that H₂0₂ is toxic in cultured mouse spinal motor neurons and selective herb extract such as Uncariae Ramulus Cum Uncis is effective in prevetion of the neurotoxicity induced by H₂O₂.

• Geomechanics and Engineering
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• v.16 no.2
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• pp.113-124
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• 2018

Under repeated loading, the residual stresses within the subgrade and subsoil can accelerate the deformation of the road structures. In this paper, a series of laboratory cyclic loading model tests and small-scale model tests were conducted to investigate the dynamic stress response within soils under different loading conditions. The experimental results showed that a dynamic stress accumulation effect occurred if the soil showed cumulative deformation: (1) the residual stress increased and accumulated with an increasing number of loading cycles, and (2) the residual stress was superimposed on the stress response of the subsequent loading cycles, inducing a greater peak stress response. There are two conditions that must be met for the dynamic stress accumulation effect to occur. A threshold state exists only if the external load exceeds the cyclic threshold stress. Then, the stress accumulation effect occurs. A higher loading frequency results in a higher rate of increase for the residual stress. In addition to the superposition of the increasing residual stress, soil densification might contribute to the increasing peak stress during cyclic loading. An increase in soil stiffness and a decrease in dissipative energy induce a greater stress transmission within the material.

• The Journal of Korean Medicine
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• v.17 no.2 s.32
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• pp.264-276
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• 1996

This study was carried out to evaluate the effect of Samhwasan on the Na-K-ATPase activity of heart muscle. The Na-K-ATPase activity was prepared from rabbit heart ventricles. Samhwasan markedly inhibited the Na- K - ATPase activity in a dose-dependent manner with an estimated $I_{50}$ of 0.56%. Hill coefficient was 1.70, indicating that the enzyme has more than one binding site for the Samhwasan. Inhibition of enzyme activity by Samhwasan increased as pretreatment time was prolonged. Inhibition by the drug was not affected by a change in enzyme protein concentration. Kinetic studies of substrate activation of the enzyme indicated classical noncompetitive inhibition, showing significant reduction in Vmax without a change in Km value. Inhibitory effect by Samhwasan was not altered by changes in concentration of $Mg^{2+}$, $Na^+$ or $K^+$, dithiothreitol. a sulfhydryl reducing reagent, did not protect the inhibition of Na-K-ATPase activity by Samhwasan combination of Samhwasan and ouabain showed a cumulative inhibition fashion. These results suggest that Samhwasan inhibits Na-K-ATPase activity of heart ventricles with an unique binding site different from that of ATP, $Mg^{2+}$, $Na^+$ or $K^+$ and ouabain.

• The Journal of Korean Medicine
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• v.30 no.6
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• pp.17-26
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• 2009

Objectives: Little information is available regarding the effect of Lycii cortex radicis (LCR) on cell viability in glioma cells. This study was therefore undertaken to examine the effect of LCR on cell survival in U87MG human glioma cells. Methods: Cell viability and cell death were estimated by MTT assay and trypan blue exclusion assay, respectively. Reactive oxygen species (ROS) generation was measured using the fluorescence probe DCFH-DA. Activation of Akt and extracellular signal-regulated kinase (ERK) and activation of caspase-3 were estimated by Western blot analysis. Results: LCR resulted in apoptotic cell death in a dose- and time-dependent manner. LCR increased reactive oxygen species (ROS) generation and LCR-induced cell death was also prevented by antioxidants, suggesting that ROS generation played a critical role in LCR-induced cell death. Western blot analysis showed that LCR treatment caused down-regulation of Akt and ERK. The LCR-induced cell death was increased by the inhibitors of Akt and ERK. Activation of caspase-3 was stimulated by LCR and caspase inhibitors prevented the LCR-induced cell death. Conclusion: These findings suggest that LCR results in human glioma cell death through a mechanism involving ROS generation, down-regulation of Akt and ERK, and caspase activation.

• BMB Reports
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• v.47 no.2
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• pp.98-103
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• 2014

Orostachys japonicus shows various biological activities. However, the molecular mechanisms remain unknown in LPS-stimulated macrophages. Here, we investigated the anti-oxidizing effect of the dichloromethane (DCM) and hexane fractions from O. japonicus (OJD and OJH) against oxidative stress in RAW 264.7 cells stimulated by LPS. OJD and OJH significantly increased the expression of heme oxygenase-1 (HO-1) in a dose- and time-dependent manner. Additionally, it was found that the expression of HO-1 was stimulated by Nrf2 activated via degradation of Keap1. ERK and p38 inhibitors repressed HO-1 induced by OJD and OJH in LPS-stimulated cells, respectively. In conclusion, these results suggest that OJD and OJH may block oxidative damage stimulated by LPS, via increasing the expression of HO-1 and Nrf2, and MAPK signaling pathway.

• Journal of Microbiology and Biotechnology
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• v.14 no.1
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• pp.121-127
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• 2004

Amphotericin B (AmB), an amphipathic polyene macrolide, is an antifungal drug produced by Streptomyces nodosus. Recently, AmB has been shown to exert antiviral activity against rubella virus and human immunodeficiency virus by different mechanisms. In this study, we evaluated the antiviral effect of AmB against Japanese encephalitis virus (JEV) and investigated which step of the viral life cycle was inhibited by AmB to understand the mechanism of antiviral action of AmB. AmB reduced both plaque size and number in the infected cells in a dose-dependent manner. In addition, a 200-fold reduction of infectious virus titer was observed by treatment of infected cells with $5\mug/ml$ of AmB. AmB acted at the post virus-infection step, but not during adsorption of virus to host cells. Western blot analysis revealed that the accumulated level of JEV envelope protein dramatically decreased in the infected cells by treatment with $5-10\mug/ml$ of AmB. Our results indicate that AmB inhibits the replication of JEV at the postinfection step by interfering with viral replication and/or by inhibiting the synthesis of viral proteins.

• Steel and Composite Structures
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• v.35 no.4
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• pp.555-566
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• 2020

This paper aims to present an analytical methodology to investigate influences of nanoscale and surface energy on buckling stability behavior of perforated nanobeam structural element, for the first time. The surface energy effect is exploited to consider the free energy on the surface of nanobeam by using Gurtin-Murdoch surface elasticity theory. Thin and thick beams are considered by using both classical beam of Euler and first order shear deformation of Timoshenko theories, respectively. Equivalent geometrical constant of regularly squared perforated beam are presented in simplified form. Problem formulation of nanostructure beam including surface energies is derived in detail. Explicit analytical solution for nanoscale beams are developed for both beam theories to evaluate the surface stress effects and size-dependent nanoscale on the critical buckling loads. The closed form solution is confirmed and proven by comparing the obtained results with previous works. Parametric studies are achieved to demonstrate impacts of beam filling ratio, the number of hole rows, surface material characteristics, beam slenderness ratio, boundary conditions as well as loading conditions on the non-classical buckling of perforated nanobeams in incidence of surface effects. It is found that, the surface residual stress has more significant effect on the critical buckling loads with the corresponding effect of the surface elasticity. The proposed model can be used as benchmarks in designing, analysis and manufacturing of perforated nanobeams.

• International Journal of Oral Biology
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• v.30 no.4
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• pp.111-116
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• 2005

Resveratrol (3,4',5-trihydroxy-trans-stilbene), a naturally occuring polyphenol compound which present in the skin of grapes and red wine has been considered to posses chemopreventive and antioxidant properties. However, little is known about the cellular actions by which resveratrol mediates its therapeutic effects. In this study, the effect of resveratrol on cell proliferation and induction of apoptosis in human osteogenic sarcoma (HOS) cells was investigated. $IC_{50}$ value was determined to be approximately $6.0{\mu}g/ml$. Chromosomal DNA framgmentation analysis showed the appearance degraded DNA in time-and dose-dependent manner upon treatment of resveratrol. In order to observe the molecular mechanism involved in resveratrol-induced apoptosis, Western blot analysis was performed. We observed the decrease in the level of procaspase-3, the zymogen form of active caspase-3 in resveratrol-treated cells. This result implies that caspase-3 is activated upon treatment of resveratrol. The activation of caspase-3 was confirmed by the cleavage of poly(ADP-ribose) polymerase. Taken together, our data demonstrate that resveratrol has anti-proliferative effect on HOS cells and induced apoptosis through activation of caspase-3 and PARP cleavage.

• Preventive Nutrition and Food Science
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• v.10 no.2
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• pp.130-133
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• 2005

The growth inhibitiory effect of chaff vinegar against various food-borne pathogenic bacteria was evaluated. Bacterial growth was evaluated in chaff vinegar at concentrations of 15, 30, 50, 65, 80, and $100\%$ using the paper disc diffusion method and 0.5, 1.0, 1.5, 1.8, 2.0, 2.2 and $2.5\%$ in broth. In the paper disc diffusion assay, chaff vinegar showed a clear zone on both the Gram-positive bacteria; Listeria monocytogenes, Staphylococcus aureus and Gram-negative bacteria; Escherichia coli O157:H7, Salmonella Typhimurium, and Vibrio parahaemolyticus. Chaff vinegar exhibited the greatest growth inhibition for V. parahaemolyticus. The bactericidal effect of chaff vinegar on the E. coli O157:H7 was tested at concentrations ranging from 0.5 to $2.5\%$ (v/v) in the LB broth media. Chaff vinegar retarded the lag phase time of the growth curve in proportion in a concentration-dependent manner. Chaff vinegar at $2.5\%$ completely inhibited the growth of E. coli O157:H7.