• Osong Public Health and Research Perspectives
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• 제9권6호
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• pp.334-339
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• 2018

Objectives: Human rhinoviruses (HRVs) are the major cause of the common cold. Currently there is no registered, clinically effective, antiviral chemotherapeutic agent to treat diseases caused by HRVs. In this study, the antiviral activity of dexamethasone (DEX) against HRV1B was examined. Methods: The anti-HRV1B activity of DEX was assessed by sulforhodamine B assay in HeLa cells, and by RT-PCR in the lungs of HRV1B-infected mice. Histological evaluation of HRV1B-infected lungs was performed and a histological score was given. Anti-HRV1B activity of DEX via the glucocorticoid receptor (GCR)-dependent autophagy activation was assessed by blocking with chloroquine diphosphate salt or bafilomycin A1 treatment. Results: In HRV1B-infected HeLa cells, treatment with DEX in a dose-dependent manner, resulted in a cell viability of > 70% indicating that HRV1B viral replication was reduced by DEX treatment. HRV1B infected mice treated with DEX, had evidence of reduced inflammation and a moderate histological score. DEX treatment showed antiviral activity against HRV1B via GCR-dependent autophagy activation. Conclusion: This study demonstrated that DEX treatment showed anti-HRV1B activity via GCR-dependent autophagy activation in HeLa cells and HRV1B infected mice. Further investigation assessing the development of topical formulations may enable the development of improved DEX effectiveness.

• Journal of Microbiology and Biotechnology
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• 제29권9호
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• pp.1349-1360
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• 2019

Chronic exposure to ultraviolet (UV) radiation, regarded as a major cause of extrinsic aging or photoaging characterized by wrinkle formation and skin dehydration, exerts adverse effects on skin by causing the overproduction of reactive oxygen species. Agastache rugosa Kuntze, known as Korean mint, possesses a wide spectrum of biological properties including anti-oxidation, anti-inflammation, and anti-atherosclerosis. Previous studies have reported that A. rugosa protected human keratinocytes against UVB irradiation by restoring the anti-oxidant defense system. However, the anti-photoaging effect of A. rugosa extract (ARE) in animal models has not yet been evaluated. ARE was orally administered to hairless mice at doses of 100 or 250 mg/kg/day along with UVB exposure for 12 weeks. ARE histologically improved UVB-induced wrinkle formation, epidermal thickening, erythema, and hyperpigmentation. In addition, ARE recovered skin moisture by improving skin hydration and transepidermal water loss (TEWL). Along with this, ARE increased hyaluronic acid levels by upregulating HA synthase genes. ARE markedly increased the density of collagen and the amounts of hydroxypoline via two pathways. First, ARE significantly downregulated the mRNA expression of matrix metalloproteinases responsible for collagen degradation by inactivating the mitogen-activated protein kinase/activator protein 1 pathway. Second, ARE stimulated the transforming growth factor beta/Smad signaling, consequently raising the mRNA levels of collagen-related genes. In addition, ARE not only increased the mRNA expression of anti-oxidant enzymes but also decreased inflammatory cytokines by blocking the protein expression of nuclear factor kappa B. Collectively, our findings suggest that A. rugosa may be a potential preventive and therapeutic agent for photoaging.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2020년도 춘계학술대회
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• pp.76-76
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• 2020

Stachys sieboldii Miq. (chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of Stachys sieboldii Miq. (SSM) in cerebral ischemia/reperfusion (I/R) injury is not yet fully understood. In the current study, the neuroblastoma cell line (SH-SY5Y) were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to simulate I/R injury in vitro model. The results showed that SSM improved OGD/R-induced inhibitory effect on cell viability of SH-SY5Y Cells. SSM displayed anti-oxidative activity as proved by the decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in OGD/R-induced SH-SY5Y Cells. In addition, cell apoptosis was markedly decreased after SSM treatment in OGD/R-induced SH-SY5Y Cells. The up-regulation of Bcl-2 and down-regulation of Bax, thus reducing the Bax/Bcl-2 ratio that in turn protected the activation of caspase-9 and -3, and inhibition of poly (ADP-ribose) polymerase cleavage, which was associated with the blocking of cytochrome c release to the cytoplasm. Collectively, SSM protected human neuroblastoma SH-SY5Y cells from OGD/R-induced injury via preventing mitochondrial-dependent pathway through scavenging excessive ROS, suggesting that SSM might be a potential agent for the ischemic stroke therapy.

• 박물관보존과학
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• 제26권
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• pp.25-34
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• 2021

문화재 복원 분야에서 3D 기술이 복원에 적용되고 있다. 그러나 아직까지 유리제 문화재의 복원에 관하여 3D 기술이 활용되어 복원된 사례가 적으며 이에 관한 연구가 필요한 상황이다. 이에 본 연구에서는 국립중앙박물관에서 소장하고 있는 보물인 금강산 출토 이성계 발원 사리장엄구 일괄 중 유리제 사리병의 결손부를 복원하는 과정에 3D 기술을 이용하였다. 보존처리는 3D 프린팅 출력물을 직접적으로 복원제로써 적용하지않고 에폭시계수지로 복제한 복원편으로 결손부를 복원하였다. 보존처리 완료 후 3D 프린팅에 사용되는 재료와 기술방식에 관하여 기존 도자기의 복원재료 중 투명성을 지닌 재료를 선택하여 사용감과 안정성을 비교하고자 하였다. 보존처리 완료 후 SLA(Stereo Lithography Apparatus)방식으로 출력한 광경화성 수지, 에폭시계 수지, 아크릴계 수지등 총 5개의 시편을 제작 한 후 96시간까지 자외선에 노출시켜 황변화를 조사하였고, 광경화성수지의 시편은 출력물에 UV차단제를 분무 여부에 따라 2종으로 나누어 자외선에 노출시켰다. 자외선 노출 결과, SLA방식 시편에 UV차단제를 분무한 시편, 에폭시계수지의 시편의 b^*값의 변화값이 1 미만으로 황변화에 안정적인 것으로 나타났으며 유리제 문화재의 복원제로써 적용 가능한 재료로 보여진다. 유리제 문화재의 형태가 매우 다양하고 복원해야할 부분 또한 다양하고 복잡하여 접근하기 어려울 수 있으므로 복원재료에 대해 여러 가지 재료를 염두해두고 고민해볼 필요가 있다.

• Journal of Chest Surgery
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• 제19권1호
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• pp.35-42
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• 1986

Prevention of thrombombolism after rosthetic cardiac valve replacement is essential for the patients. About 90% of patients are free of major and minor thromboembolic complications 5 year after replacement of cardiac valves with prosthetic devices when they are under control of anticoagulant therapy. Ticlopidine is a drug that alter platelet function to have an antithrombotic effect. It is an antiaggregating agent which inhibits primary platelet function to have an antithrombotic effect. It is an antiaggregating agent which inhibits primary platelet aggregation induced by ADP and increases the production of prostaglandin $D_{2}$. Aspirin in small doses inhibits platelet synthesis of prostaglandins by irreversibly blocking the enzyme cyclo-oxygenase. Platelet secretion and aggregation are impaired with Ticlopidine and Aspirin. the thromboembolic event sof 54 patient s who were treated with Ticlopidine and Aspirin after cardiac valve replacement were evaluated and compared with that of 79 patients who were treated with Wafarin and Aspirin after the same type of operation. The follow-up period ranged from 4 to 110 months (mean of 48 months). there were 11 major thromboembolic episodes including three deaths in the warfarin goup during mean follow-up period of 56 months. two cases of CVA and one hemoarthrosis were noted due to overdose of Warfarin. Inticlopidine group, there was only one fatal thromboembolic epdisode three month after mitral valve replacement during mean follow-up period of 18 months. Two episodes of hypermenorrhea resulting anemia ere noted in the ticlopidine group. We measured the parameters of platelet function in aggreagation curve of platelet with platelet aggregometer (chrono-log Aggregometer, Model No. 430) Aggregation test was performed with three final concentrations of epinephrine in 10 uM/L, ADP in 5uM/L. 28 patients with prosthetic cardiac valves and 35 healthy volunteers were subgrouped as follows to analyze the effect of antithrombotic drugs used. Group I ; 11 patients treated with 250-500 mg of ticlopidine and 0.5gm of Aspirin as a daily single dose after cardiac valve replacement (14 St. Jude Medical and 1 Carpentier-Edwards, 9 patients with atrial fibrillation among them) Group II ; 10 patients treated with 3-5 mg of Warfarin and 0.75 gm of Aspirin daily to prolong prothrombin time around 20 seconds for more than 6 months and single Aspirin dose was maintained afterward as a life-long regimes(3 St. Jude Medical, 1 Hall-Kaster and 7 Carpentier-Edwards valve, 9 patients in atrial fibrilation). Group III ; 7 patients who quit anticoagulant treatment (Warfarin + Aspirin) 6-12 months after the regime as group II (3 St. Jude Medical. 1 bjork-Shiley, 1 Hall-Kaster, 3 Carpentier-Edwards valve, 2 of them are with atrial fibrillation). Group IV ; 35 healthy vounteers (28 males and 7 females). The following results were obtained. 1. The mean maximal platelet aggregability in Group I induced by 10uM/L epinephrine was 15.6%, and 17.5 and 18.7% in BM in proportion to the induction by 5 and 10 uM/L ADP. 2. The mean maximal platelet aggregability in Group II induced by 10uM/L epinephrine was 16.5%, and 27.4 and 44.7% in BM in proportion to the induction by 5 and 10uM/L ADP. 3. The mean maximal platelet aggregability in group III induced by 10uM/L epinephrine was 65%, and 56.5 and 51.8% in BM in proportion to the induction by 5 and 10 uM/L ADP. 4. The mean maximal platelet aggregability in the normal subjects induced by 10 uM/L epinephrine was 64%, and 65 and 69% in Bm inproportion to the induction by 5 and 10 uM/L ADP. 5. Reversible change of platelet aggregation curve induced by 5 and 10uM/L was noted all of the patients in Group I. conclusion : Ticlopidine is an antiaggregating agent which inhibits primary platelet aggregation induced by ADP, and increases the production of prostaglandin $D_{2}$. Ticlopidine and Aspirin produced a significant inhibition of platelet in the presence of ADP and epinephrine in our study. Acccording to our brief experience, 250 mg of ticlopidine and low dose of Aspirin resulted synergistic superior effect to each drug alone in prevention of thromboembolism after prosthetic cardiac valve replacement.

• Journal of Microbiology and Biotechnology
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• 제25권10호
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• pp.1751-1760
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• 2015

Mucin2 (MUC2), an important regulatory factor in the immune system, plays an important role in the host defense system against bacterial translocation. Probiotics known to regulate MUC2 gene expression have been widely studied, but the interactions among probiotic, pathogens, and mucin gene are still not fully understood. The aim of this study was to investigate the role of MUC2 in blocking effects of probiotics on meningitic E. coli-induced pathogenicities. In this study, live combined probiotic tablets containing living Bifidobacterium, Lactobacillus bulgaricus, and Streptococcus thermophilus were used. MUC2 expression was knocked down in Caco-2 cells by RNA interference. 5-Aza-2'-deoxycytidine (5-Aza-CdR), which enhances mucin-promoted probiotic effects through inducing production of Sadenosyl-L-methionine (SAMe), was used to up-regulate MUC2 expression in Caco-2 cells. The adhesion to and invasion of meningitic E. coli were detected by competition assays. Our studies showed that probiotic agents could block E. coli-caused intestinal colonization, bacteremia, and meningitis in a neonatal sepsis and meningitis rat model. MUC2 gene expression in the neonatal rats given probiotic agents was obviously higher than that of the infected and uninfected control groups without probiotic treatment. The prohibitive effects of probiotic agents on MUC2-knockdown Caco-2 cells infected with E44 were significantly reduced compared with nontransfected Caco-2 cells. Moreover, the results also showed that 5-Aza-CdR, a drug enhancing the production of SAMe that is a protective agent of probiotics, was able to significantly suppress adhesion and invasion of E44 to Caco-2 cells by upregulation of MUC2 expression. Taken together, our data suggest that probiotic agents can efficiently block meningitic E. coli-induced pathogenicities in a manner dependent on MUC2.

• 공업화학
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• 제33권2호
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• pp.173-178
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• 2022

탄소나노점@실리카를 신호 형질 소재로 이용한 측면 유동 면역 형광 분석법을 개발하여 폐암 바이오마커 중에 하나인 레티놀 결합 단백질 4의 농도를 분석하는 데 적용하고자 하였다. 측면 유동 면역 형광 분석법에서 항원 검출을 위해 바이오리셉터로 주로 사용하였던 항체 대신 좀 더 경제적이고, 장기간 보관성이 용이하며, 특정 표적 단백질에 대해 친화력이 강한 압타머를 니트로셀룰로오스 멤브레인에 사용하였다. 레티놀 결합 단백질 4에 특이적이며 5' 말단을 비오틴으로 변형한 압타머를 뉴트라비딘과 반응시켜 비오틴과 뉴트라비딘의 강한 결합력에 의해 압타머가 니트로 셀룰로오스 멤브레인에 고정되도록 하였다. 압타머가 고정된 스트립에 레티놀 결합 단백질 4 항체를 공유결합으로 고정한 탄소나노점@실리카 블루 형광 신호 형질 나노입자와 레티놀 결합 단백질 4 항원을 측면 유동 방식으로 흘려 주어 샌드위치 복합체를 형성하였다. 이렇게 형성된 샌드위치 복합체에서 탄소나노점@실리카 나노입자에 의한 형광 신호를 측정하여 항원 농도를 분석하기 위한 최적의 조건을 선정하기 위해 전개 완충용액에 첨가된 계면활성제의 농도, 이온 세기를 변화시키면서 블로킹 시약을 추가적으로 사용하였다. 그 결과 150 mM NaCl 및 0.05% Tween-20을 포함하는 10 mM Tris 완충용액(pH 7.4)에서 0.6 M 에탄올아민을 블로킹 시약으로 사용하였을 때 니트로셀룰로오스 멤브레인에 도포된 압타머와 레티놀 결합 단백질 4 항원 및 탄소나노점@실리카 나노입자로 레이블링한 항체가 결합하여 최적의 형광분석신호를 내는 것을 확인 가능하였다. 이러한 결과는 현장진단검사 키트로 현재 각광을 받고 있는 측면 유동 면역 형광 분석법에서 항체 대신 압타머를 니트로셀룰로오스 멤브레인에 고정함으로써 좀 더 경제적이며, 장기간 보관이 용이한 측면 유동 면역 형광 분석 칩을 제작하여 폐암 질환 진단용 바이오마커 검출이 가능함을 시사하였다.

• 생명과학회지
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• 제28권8호
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• pp.885-891
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• 2018

급성위막성대장염(Pseudomembranous colitis)은 C. difficile 세균이 분비하는 톡신A에 의해 유발되는 것으로 알려져 있다. 톡신A에 의한 점막 상피세포의 장벽기능 감소가 발병 원인으로 알려져 있다. 최근 연구에 의하면 톡신 A는 대장상피세포 속 HDAC-6의 활성을 높여 튜블린의 탈아세틸화를 증가시키는 것으로 알려져 있다. 튜블린 단백질의 탈아세틸화는 미세소관 불 형성을 초래하여 점막 상피세포의 극단적인 세포 형태 변형을 야기하게 되며 결국 상피세포의 고유기능인 장벽 기능이 파괴된다고 알려져 있다. 최근 연구자 등은 potassium acetate가 톡신A에 의한 튜블린 탈아세틸화와 미세소관 불 형성을 회복시켜 장염을 유의하게 억제함을 보고하였다. 따라서 본 연구에서는 아세틸기를 포함하는 또 다른 간단한 화학구조의 초산을 적용하여 톡신A의 세포독성을 억제하는지 확인해보고자 하였다. 인간 대장상피세포에서 초산 자극은 튜블린 단백질의 아세틸화를 유의하게 증가시켰다. 또한 초산은 대장상피세포 속 미세소관 형성과정도 강하게 촉진시킴을 확인하였다. 초산은 톡신A에 의한 튜블린 탈아세틸화와 미세소관 불 형성 그리고 세포독성 모두를 유의하게 회복시켰다. 이상의 결과는 초산에 의한 미세소관 형성 촉진이 톡신A에 의해 초래되는 세포골격계 파괴와 그로 인한 세포독성을 억제할 수 있음을 보여준다. 따라서 초산이 톡신A의 작용을 차단하여 위막성대장염 증상을 완화시킬 수 있는 치료제로서 개발 가치가 있음을 보여준다.

• IMMUNE NETWORK
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• 제1권3호
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• pp.213-220
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• 2001

Background: A previous study has shown that Euonymus alatus (EA) has an antidotic activities against inflammation, suggesting possibility that EA can exert this beneficial effects to liver injury by an initial protection against drug-induced hepatocyte demage. The present study was undertaken to evaluate the protective effect of EA-extract on experimentally induced hepatitis in ICR mice and to investigate some mechanisms responsible for its action. Methods: Water EA extract was used in this experiments. The mice received i.p. a dose of 700 mg/kg galactosamine (GalN) together with $5{\mu}g/kg$ of endotoxin (LPS), or received i.v. 12 mg/kg of concanavalin A (Con A). EA (4 mg/mouse) was administrated on day -2, -1 and 0 before induction of liver injury. Liver injury was assessed by measurement of serum alanin amino-transferase (SGPT) levels on 9 hr after GaIN.LPS, or 8 hr after con A administration. Results: Treatment with either GaIN or LPS alone did not cause hepatitis. However, simultaneous administration of GalN and LPS to mice resulted in LPS-dose dependent fulminant hepatitis. GaLN/LPS-induced liver injury was reduced when mice were given EA for 3 days before induction. This preventive effect of Ea was more prominent when EA was given by intraperitoneal route rather then by oral route. Pretreatment of EA or dexamethasone inhibited significantly $TNF{\alpha}$ production in GalL/LPS-injured mice. However, EA-treatment did not influence $TNF{\alpha}$-induced hepatitis in GalN-sensitized mice, suggesting that $TNF{\alpha}$ is likely to act as one of final mediators of endotoxin action and the protective effect of EA might be manifested chiefly by inhibition of endotoxin-induced $TNF{\alpha}$ production, not by blocking the $TNF{\alpha}$-action. Injection of Con A into mice evoked remarkable liver injury in a dose dependent fashion. This liver damage was reduced by EA-pretreatment. Dexamethasone significantly reduced both GalL/LPS-induced and Con A-induced liver damages, showing synergism with EA. However, indomethacin reduced only GalN/ LPS-induced hepatitis, not for Con A-induced hepatitis. Conclusion: These results led to the conclusion that EA may be able to contribute at least in part to prevent the drug-induced hepatotoxicity, and that its anti-hepatitis effects might be manifested directly by modulation of endogenous mediators, such as leukotriese D4, $TNF{\alpha}$ and free radical, and indirectly by regulation of immune mediated responses. Also these results suggested that EA could be developed as a potential antidotic agent.

• BMB Reports
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• 제51권11호
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• pp.572-577
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• 2018

Recent studies showed that the PD-1/PD-L1 checkpoint blockade is a dramatic therapy for melanoma by enhancing antitumor immune activity. Currently, major strategies for the PD-1/PD-L1 blockade have mainly focused on the use of antibodies and compounds. Seeking an alternative approach, others employ endogenous proteins as blocking agents. The extracellular domain of PD-1 (ePD1) includes the binding site with PD-L1. Accordingly, we constructed a PD-1-based recombinantly tailored fusion protein (dFv-ePD1) that consists of bivalent variable fragments (dFv) of an MMP-2/9-targeted antibody and ePD1. The melanoma-binding intensity and antitumor activity were also investigated. We found the intense and selective binding capability of the protein dFv-ePD1 to human melanoma specimens was confirmed by a tissue microarray. In addition, dFv-ePD1 significantly suppressed the migration and invasion of mouse melanoma B16-F1 cells, and displayed cytotoxicity to cancer cells in vitro. Notably, dFv-ePD1 significantly inhibited the growth of mouse melanoma B16-F1 tumor cells in mice and in vivo fluorescence imaging showed that dFv-ePD was gradually accumulated into the B16-F1 tumor. Also the B16-F1 tumor fluorescence intensity at the tumor site was stronger than that of dFv. This study indicates that the recombinant protein dFv-ePD1 has an intensive melanoma-binding capability and exerts potent therapeutic efficacy against melanoma. The novel format of the PD-L1-blocked agent may play an active role in antitumor immunotherapy.