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Shin, M.J.,Kim, D.W.,Jo, H.S.,Cho, S.B.,Park, J.H.,Lee, C.H.,Yeo, E.J.,Choi, Y.J.,Kim, J.A.,Hwang, J.S.,Sohn, E.J.,Jeong, J.H.,Kim, D.S.,Kwon, H.Y.,Cho, Y.J.,Lee, K.,Han, K.H.,Park, J.,Eum, W.S.,Choi, Pergamon ; Elsevier Science Ltd 2016 FREE RADICAL BIOLOGY AND MEDICINE Vol.97 No.-
Proline rich Akt substrate (PRAS40) is a component of mammalian target of rapamycin complex 1 (mTORC1) and is known to play an important role against reactive oxygen species-induced cell death. However, the precise function of PRAS40 in ischemia remains unclear. Thus, we investigated whether Tat-PRAS40, a cell-permeable fusion protein, has a protective function against oxidative stress-induced hippocampal neuronal (HT-22) cell death in an animal model of ischemia. We showed that Tat-PRAS40 transduced into HT-22 cells, and significantly protected against cell death by reducing the levels of H<SUB>2</SUB>O<SUB>2</SUB> and derived reactive species, and DNA fragmentation as well as via the regulation of Bcl-2, Bax, and caspase 3 expression levels in H<SUB>2</SUB>O<SUB>2</SUB> treated cells. Also, we showed that transduced Tat-PARS40 protein markedly increased phosphorylated RRAS40 expression levels and 14-3-3σ complex via the Akt signaling pathway. In an animal ischemia model, Tat-PRAS40 effectively transduced into the hippocampus in animal brain and significantly protected against neuronal cell death in the CA1 region. We showed that Tat-PRAS40 protein effectively transduced into hippocampal neuronal cells and markedly protected against neuronal cell damage. Therefore, we suggest that Tat-PRAS40 protein may be used as a therapeutic protein for ischemia and oxidative stress-induced brain disorders.
Park, S.J.,Si, Y.J.,Kim, J.,Song, M.S.,Kim, S.m.,Kim, E.H.,Kwon, H.i.,Kim, Y.I.,Lee, O.J.,Shin, O.S.,Kim, C.J.,Shin, E.C.,Choi, Y.K. Academic Press 2016 Virology Vol.498 No.-
<P>To investigate cross-protective vaccine efficacy of highly-pathogenic avian influenza H5N1 viruses against a recent HPAI H5N8 virus, we immunized C57BL/6 mice and ferrets with three alum-adjuvanted inactivated whole H5N1 vaccines developed through reverse-genetics (Rg): [Vietnam/1194/04xPR8 (clade 1), Korea/W149/06xPR8 (clade 2.2), and Korea/ES223N/03xPR8 (clade 2.5)]. Although relatively low cross-reactivities (10-40 HI titer) were observed against heterologous H5N8 virus, immunized animals were 100% protected from challenge with the 20 mLD(50) of H5N8 virus, with the exception of mice vaccinated with 3.5 mu g of Rg Vietnam/1194/04xPR8. Of note, the Rg Korea/ES223N/03xPR8 vaccine provided not only effective protection, but also markedly inhibited viral replication in the lungs and nasal swabs of vaccine recipients within five days of HPAI H5N8 virus challenge. Further, we demonstrated that antibody-dependent cell-mediated cytotoxicity (ADCC) of an antibody-coated target cell by cytotoxic effector cells also plays a role in the heterologous protection of H5N1 vaccines against H5N8 challenge. (C) 2016 Elsevier Inc. All rights reserved.</P>
Park, Y-H,Kim, S-U,Kwon, T-H,Kim, J-M,Song, I-S,Shin, H-J,Lee, B-K,Bang, D-H,Lee, S-J,Lee, D-S,Chang, K-T,Kim, B-Y,Yu, D-Y Macmillan Publishers Limited 2016 Oncogene Vol.35 No.27
<P>The current study was carried out to define the involvement of Peroxiredoxin (Prx) II in progression of hepatocellular carcinoma (HCC) and the underlying molecular mechanism(s). Expression and function of Prx II in HCC was determined using H-ras(G12V)-transformed HCC cells (H-ras(G12V)-HCC cells) and the tumor livers from H-ras(G12V)-transgenic (Tg) mice and HCC patients. Prx II was upregulated in H-ras(G12V)-HCC cells and H-ras(G12V)-Tg mouse tumor livers, the expression pattern of which highly similar to that of forkhead Box M1 (FoxM1). Moreover, either knockdown of FoxM1 or site-directed mutagenesis of FoxM1-binding site of Prx II promoter significantly reduced Prx II levels in H-ras(G12V)-HCC cells, indicating FoxM1 as a direct transcription factor of Prx II in HCC. Interestingly, the null mutation of Prx II markedly decreased the number and size of tumors in H-ras(G12V)-Tg livers. Consistent with this, knockdown of Prx II in H-ras(G12V)-HCC cells reduced the expression of cyclin D1, cell proliferation, anchorage-independent growth and tumor formation in athymic nude mice, whereas overexpression of Prx II increased or aggravated the tumor phenotypes. Importantly, the expression of Prx II was correlated with that of FoxM1 in HCC patients. The activation of extracellular signal-related kinase (ERK) pathway and the expression of FoxM1 and cyclin D1 were highly dependent on Prx II in H-ras(G12V)-HCC cells and H-ras(G12V)-Tg livers. Prx II is FoxM1-dependently- expressed antioxidant in HCC and function as an enhancer of Ras(G12V) oncogenic potential in hepatic tumorigenesis through activation of ERK/FoxM1/cyclin D1 cascade.</P>
H. pylori 제균 실패율과 clarithromycin 내성률의 일치성
허재형 ( J. H. Heo ),남승우 ( S. W. Nam ),노임환 ( I. H. Roe ),양미라 ( M. R. Yang ),김정택 ( J. T. Kim ),송일환 ( I. H. Song ),임창영 ( C. Y. Lim ),김정원 ( J. W. Kim ),신지현 ( J. H. Shin ) 대한소화기학회 2002 대한소화기학회 춘계학술대회 Vol.2002 No.-
<목적> H. pylori 제균 치료성적을 좌우하는 요소에는 약제와 대상 환자군의 선정, 균검사방법의 차이, 항생제 저항성 등이 중요시되고 있다. 이 중에서도 항생제 저항성은 나라간의 H. pylori 제균 성적을 다르게 하는 대표적인 원인이다. 우리나라는 제균률이 외국보다 저조하여 85%내외로 보고되고 있다. 본 연구의 목적은 H. pylori 제균 실패율과 clarithromycin 내성률을 조사하여 제균 실패 원인으로서의 clarithromycin
Shin, J.Y.,Bae, G.S.,Choi, S.B.,Jo, I.J.,Kim, D.G.,Lee, D.S.,An, R.B.,Oh, H.,Kim, Y.C.,Shin, Y.K.,Jeong, H.W.,Song, H.J.,Park, S.J. Elsevier Science 2015 INTERNATIONAL IMMUNOPHARMACOLOGY Vol.29 No.2
We previously reported that Nardostachys jatamansi (NJ) exhibits anti-inflammatory activity against lipopolysaccharide (LPS). However, the active compound in NJ is unknown. Therefore, here, we examined the effects of desoxo-narchinol-A (DN) isolated from NJ against LPS-induced inflammation. To demonstrate the anti-inflammatory effect of DN against LPS, we used two models; murine endotoxin shock model for in vivo model, and peritoneal macrophage responses for in vitro. In endotoxin shock model, DN was administrated intraperitoneally 1h before LPS challenge, then we evaluated mice survival rates and organ damages. Pretreatment with DN (0.05mg/kg, 0.1mg/kg, or 0.5mg/kg) dramatically reduced mortality in a murine LPS-induced endotoxin shock model. Furthermore, DN inhibited tissue injury and production of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α), in the liver and lung. In in vitro macrophage model, we examined the inflammatory mediators and regulatory mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB). DN inhibited the production of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and its derivative nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>), IL-1β, IL-6 and TNF-α and H3 protein acetylation in murine peritoneal macrophages. DN also inhibited p38 activation, but not extracellular signal-regulated kinase (ERK), c-jun NH<SUB>2</SUB>-terminal kinase (JNK), and NF-κB. These results suggest that DN from NJ exhibits protective effects against LPS-induced endotoxin shock and inflammation through p38 deactivation.
H. pylori성 위염에서 위축진행과 Myeloperoxidase(MPO) 유전자 다형성(genetic polymorphism)의 관련성
이만용 ( M. Y. Lee ),노임환 ( I. H. Roe ),양미라 ( M. R. Yang ),남승우 ( S. W. Nam ),허재형 ( J. H. Heo ),임창영 ( C. Y. Lim ),송일한 ( I. H. Song ),김정원 ( J. W. Kim ),신지현 ( J. H. Shin ) 대한소화기학회 2002 대한소화기학회 춘계학술대회 Vol.2002 No.-
<목적> H. pylori는 위 점막에서 많은 중성구들의 침윤이 특징적으로 관찰되는 활동성 위염을 일으키며 중성구들에서 나오는 많은 산소라디칼 등은 상피세포의 손상과 apoptosis을 유도하고 위축성 변화로 진전하는데 주도적인 역할을 한다. 특히 중성구의 myeloperioxidase(MPO)는 산소라디칼의 공격적인 산화적 잠재력을 중폭시키고 monochloramine을 생성하여 위세포의 손상과 위축성 변화를 야기한다고 이해되고 있다. 그러나 위축성위
Ceruloplasmin is an endogenous protectant against kainate neurotoxicity
Shin, E.J.,Jeong, J.H.,Chung, C.K.,Kim, D.J.,Wie, M.B.,Park, E.S.,Chung, Y.H.,Nam, Y.,Tran, T.V.,Lee, S.Y.,Kim, H.J.,Ong, W.Y.,Kim, H.C. Pergamon ; Elsevier Science Ltd 2015 FREE RADICAL BIOLOGY AND MEDICINE Vol.84 No.-
To determine the role of ceruloplasmin (Cp) in epileptic seizures, we used a kainate (KA) seizure animal model and examined hippocampal samples from epileptic patients. Treatment with KA resulted in a time-dependent decrease in Cp protein expression in the hippocampus of rats. Cp-positive cells were colocalized with neurons or reactive astrocytes in KA-treated rats and epileptic patient samples. KA-induced seizures, initial oxidative stress (i.e., hydroxyl radical formation, lipid peroxidation, protein oxidation, and synaptosomal reactive oxygen species), altered iron status (increasing Fe<SUP>2+</SUP> accumulation and L-ferritin-positive reactive microglial cells and decreasing H-ferritin-positive neurons), and impaired glutathione homeostasis and neurodegeneration (i.e., Fluoro-Nissl and Fluoro-Jade B staining analyses) were more pronounced in Cp antisense oligonucleotide (ASO)- than in Cp sense oligonucleotide-treated rats. Consistently, Cp ASO facilitated KA-induced lactate dehydrogenase (LDH) release, Fe<SUP>2+</SUP> accumulation, and glutathione loss in neuron-rich and mixed cultures. However, Cp ASO did not alter KA-induced LDH release or Fe<SUP>2+</SUP> accumulation in the astroglial culture, but did facilitate impairment in glutathione homeostasis in the same culture. Importantly, treatment with human Cp protein resulted in a significant attenuation against these neurotoxicities induced by Cp ASO. Our results suggest that Cp-mediated neuroprotection occurs via the inhibition of seizure-associated oxidative damage (including impairment in glutathione homeostasis), Fe<SUP>2+</SUP> accumulation, and alterations in ferritin immunoreactivity. Moreover, interactive modulation between neurons and glia was found to be important for Cp upregulation in the attenuation of epileptic damage in both animals and humans.