Anti-inflammatory and Anti-oxidant Effects of PHBV/Collagen (PHCP) on Lipopolysaccharide-Induced Skin Inflammation

Jin-Yi Han3*, Xu Zi Guang, Jyung-Sik Kwak, Ki-Wan Oh, Han-Ik Bae 충북대학교 동물의학연구소 2012 Journal of Biomedical and Translational Research Vol.13 No.1

The anti-inflammatory effect of PHBV/Collagen (PHCP) was examined in a mouse model of lipopolysaccharide (LPS)-induced skin inflammation. Vascular permeability on the back skin was measured by the local accumulation of Evan’s blue dye after subcutaneous injection of LPS (30 μg site-1). Dye leakage in the skin showed a significant increase at 2 h after injection of LPS. This LPS-induced dye leakage was also completely inhibited by HO-1 inhibitor, ZnPP, and antioxidants, including methyl gallate, trolox, and mannitol. To study the possible mechanisms underlying the in vivo anti-inflammatory effect of PHCP against LPS-induced inflammation, we also examined the effects of PHCP on malondialdehyde (MDA) and glutathione levels in skin tissues and found that pretreatment with PHCP resulted in inhibited MDA elevation and a remarkable reduction of glutathione level. In addition, similar results were obtained after pretreatment with antioxidants, including trolox and mannitol, and HO-1 inhibitor, ZnPP. Histopathologically, an influx of neutrophils into the skin dermis was detected between 24 h and 72 h after LPS injection (30, 100 μg site-1), compared to control animals after injection of saline. This increase was greater in mice treated with 100 μg of LPS than in those treated with 30 μg of LPS and was significantly suppressed by pretreatment with PHCP, antioxidants, and HO-1 inhibitor. These results collectively suggest that PHCP has an anti-inflammatory effect against LPS-induced inflammation model in vivo and may be a good candidate for the skin tissue engineering biomedical application primarily through manipulation of the redox state.

單症性 健康念慮症의 臨床經驗

韓辰熙,柳太烈,趙伯紀,李鍾六 서울醫大 1990 精神醫學 Vol.15 No.2

Four new compounds from the bulbs of Lycoris aurea with neuroprotective effects against CoCl2 and H2O2-induced SH-SY5Y cell injuries

An Jin,Xuelian Xiang,Yun-Yun Zhu,Heng-Yi Yu,Hui-Fang Pi,Peng Zhang,Han-Li Ruan 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.3

Three new alkaloids, 2a-hydroxy-6-O-n-butyloduline,O-n-butyllycorenine, (-)-N-(chloromethyl)lycoramine(1–3), and a new phenolic compound, ((7S)-7-(4-hydroxyphenyl)-7-hydroxypropyl)-20-methylbenzene-30,60-diol (14), along with ten known alkaloids (4–13), wereisolated from the bulbs of Lycoris aurea collected fromHuaihua County of Hunan Province, China. Their structureswere elucidated by spectroscopic methods includingHRESIMS, UV, IR, and NMR. All the isolated compoundswere tested for their neuroprotective effects against CoCl2and H2O2-induced SH-SY5Y cell death. Compounds 1–7and 10 exhibited significant neuroprotective effects againstCoCl2-induced SH-SY5Y cell injury, while compounds1–5, 7, 10 and 12 showed obvious neuroprotective effectsagainst H2O2-induced SH-SY5Y cell death.

보행속력과 동작의 부드러움과의 상관관계에 관한 연구

탁계래,한영민,최진승,이정한,임영태,전재훈,박상균,박승하,Stefanyshin Darren 한국운동역학회 2006 한국운동역학회지 Vol.16 No.1

저크비용함수를 이용한 골프 숙련자와 초보자간의 퍼팅 동작 분석

임영태,최진승,한영민,김형식,이정한,전재훈,탁계래 한국운동역학회 2006 한국운동역학회지 Vol.16 No.1

『남양선생시집』 간행과 『고려대장경』 조성사업

최연주 ( Choi Yeon-joo ),전진이 ( Jun Jin-yi ),한홍익 ( Han Hong-ik ) 한국밀교학회 2022 불교학밀교학연구 Vol.1 No.-

『남양선생시집』은 고려 무인집권기에 문신관료였던 백분화의 시집이다. 그는 스스로 參禪居士라 할 정도로 禪法을 좋아하였다. 이 시집은 백분화의 장남인 희심이 간행을 주도하였다. 승려이자 문인이었던 희심은 부친이 생전에 남긴 시 2백여 首를 수습해 上下卷으로 편찬하고, 제목과 서문을 이규보 아들인 이함에게 의뢰하였다. 백분화는 이규보보다 나이가 10살 적었지만 일찍 出仕하였다. 최씨정권과 밀착되었던 백분화는 이규보의 출사를 위해 다방면으로 도움을 주었을 것이다. 이는 두 사람이 주고 받은 詩와 이규보가 지은 백분화의 묘지명을 통해 충분히 짐작할 수 있다. 이러한 두 사람의 관계는 아들인 희심과 이함에게 자연스럽게 이어져 시집의 제목과 서문 작성 배경이 되었을 것이다. 『남양선생시집』은 『고려대장경』 조성사업이 마무리된 직후인 고종 36년(1249)에 간행되었다. 시집에서 惠堅과 孝眞이라는 각수가 조사되었는데, 이들은 『고려대장경』 판각에 참여한 각수이다. 시집 간행이 『고려대장경』 판각과 밀접하게 연관되어 있음을 보여준다. 『남양선생시집』 간행 과정을 검토해 보면 이규보의 『동국이상국집』 간행과 유사한 점이 많다. 그렇다면 『고려대장경』 조성사업의 체계를 활용하여 분사대장도감(이하 분사도감으로 약칭함)에서 『남양선생시집』을 간행하였을 개연성이 매우 높다. 『Namyang Seonsaeng Sijib』(『南陽先生詩集』) is a collection of Beak Bunhwa(白賁華) in a period of the Choi military regime. He had continuously interchanged with the Buddhist community including reputed monks. 『Namyang Seonsaeng Sijib』 was published by monk Huisim(希諗), the eldest son of Beak Bunhwa. Twenty-five years after the death of his father, Huisim had collected scattered poems and compiled them into two volumes. Yi Ham(李涵), the son of Yi Gyubo(李奎報), wrote the preface of it. Likewise, Yi Gyubo wrote the epitaph of Beak Bunhwa. Beak Bunhwa and Yi Gyubo were deeply involved in politics and literature. To sum up this causality, these two families had a quite friendly relationship. Meanwhile, 『Namyang Seonsaeng Sijib』 was released immediately after the engraving of 『Tripitaka Koreana』. Hyegyeon(惠堅) and Hyojin(孝眞), engravers who participated in the engraving 『Tripitaka Koreana』, undertook repeatedly the editing of 『Namyang Seonsaeng Sijib』. It shows that publication of 『Namyang Seonsaeng Sijib』 and engraving of 『Tripitaka Koreana』 are closely linked. Beak Bunhwa and Yi Gyubo are politicians who cooperated with the Choi military regime. As 『Donggukyisanggukjip』(『東國李相國集』), the collection of Yi Gyubo, was produced in Bunsadogam(分司都監) with the support of King Gojong and the Choi military regime, it is highly likely that 『Namyang Seonsaeng Sijib』 was produced in the same time.

β-Cell-protective effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid as a glutamate dehydrogenase activator in db/db mice.

Han, Seung Jin,Choi, Sung-E,Yi, Sang-A,Lee, Soo-Jin,Kim, Hae Jin,Kim, Dae Jung,Lee, Hyun Chul,Lee, Kwan Woo,Kang, Yup Journal of Endocrinology, Ltd. [etc.] 2012 The Journal of endocrinology Vol.212 No.3

<P>2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) is an activator of glutamate dehydrogenase (GDH), which is a mitochondrial enzyme with an important role in insulin secretion. We investigated the effect of BCH on the high-glucose (HG)-induced reduction in glucose-stimulated insulin secretion (GSIS), the HG/palmitate (PA)-induced reduction in insulin gene expression, and HG/PA-induced β-cell death. We also studied whether long-term treatment with BCH lowers blood glucose and improves β-cell integrity in db/db mice. We evaluated GSIS, insulin gene expression, and DNA fragmentation in INS-1 cells exposed to HG or HG/PA in the presence or absence of BCH. An in vivo study was performed in which 7-week-old diabetic db/db mice were treated with BCH (0.7? g/kg, n = 10) and placebo (n = 10) every other day for 6 weeks. After treatment, an intraperitoneal glucose tolerance test and immunohistological examinations were performed. Treatment with BCH blocked HG-induced GSIS inhibition and the HG/PA-induced reduction in insulin gene expression in INS-1 cells. In addition, BCH significantly reduced HG/PA-induced INS-1 cell death and phospho-JNK level. BCH treatment improved glucose tolerance and insulin secretion in db/db mice. BCH treatment also increased the ratio of insulin-positive β-cells to total islet area (P < 0.05) and reduced the percentage of β-cells expressing cleaved caspase 3 (P < 0.05). In conclusion, the GDH activator BCH improved glycemic control in db/db mice. This anti-diabetic effect may be associated with improved insulin secretion, preserved islet architecture, and reduced β-cell apoptosis.</P>

Non-invasive Measurement of Radical Reaction and Pharmacokinetic Study of Nitroxyl Probe in Lung of Living Mice Using In vivo ESR Spectroscopy

Jin-Yi Han, Hideo Utsumi 충북대학교 동물의학연구소 2011 Journal of Biomedical and Translational Research Vol.12 No.1

We investigated free radical reactions in lung of living mice using an in vivo electron spin resonance (ESR) spectrometer and nitroxyl radical as a probe. When an aqueous solution of nitroxyl probe was trans-tracheally administered into lung of living mice, a sharp triplet signal was observed at the chest of the mice. The signal showed a gradual decrease with time, obeying first-order kinetics. Signal decay rates of carbamoyl-PROXYL and carboxy-2,2,6,6-tetramethyl-piperidine-N-oxyl were faster than those of CAT-1 and carboxy-PROXYL. The mechanism of signal decay may be attributed to (i) reaction with reactive oxygen species such as ·OH, (ii) transfer into blood circulation, or (iii) reduction by compounds continuously supplied. However, little is known about the clearance mechanism of the nitroxyl probe in lung. To evaluate the disappearance of the ESR signal of the nitroxyl probe in lung, in vivo ESR spectra in chest of mice was recorded after trans-tracheal administration of an aqueous high concentrate solution of nitroxyl probe. A broad signal from the chest was observed immediately after administration due to Heisenberg spin exchange interaction. A sharp triplet signal was superimposed on the broad signal and the appearance of a triplet signal was followed by disappearance of the broad one. Peak-to-peak line width of the sharp signal was almost the same as that after intravenous administration. A distinct signal was detected in blood collected 10 min after trans-tracheal administration of nitroxyl probe. The observations indicate the transfer from lung to blood circulation and its contribution to clearance of probe in lung. Appearance of a sharp signal in blood after trans-tracheal administration was dependent on the kind of nitroxyl probe, showing a different transfer rate from lung to blood.

Flavonoids and Their Free Radical Reactions

Jin-Yi Han, Jin-Tae Hong, Sang-Yoon Nam, Ki-Wan Oh 충북대학교 동물의학연구소 2009 Journal of Biomedical and Translational Research Vol.10 No.2

본문참고

Plasma leptin concentrations are greater in type II diabetic patients and stimulate monocyte chemotactic peptide-1 synthesis via the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway

( Jin Joo Cha ),( Young Youl Hyun ),( Yi Hwa Jee ),( Mi Jin Lee ),( Kum Hyun Han ),( Young Sun Kang ),( Sang Youb Han ),( Dae Ryong Cha ) 대한신장학회 2012 Kidney Research and Clinical Practice Vol.31 No.3

Background: Leptin is an adipokine that is recently reported to be a biomarker of systemic inflammation. Although atherosclerosis causes cardiovascular diseases, it is not clear whether leptin contributes to the acceleration of this process. In this study, we investigated whether alterations of plasma leptin levels were related to diabetic nephropathy and systemic inflammation. In addition, we examined the physiologic action of leptin in cultured vascular smooth muscle cells (VSMCs). Methods: A total of 126 type 2 diabetic participants and 37 healthy controls were studied. The diabetic participants were divided into three groups according to stage of nephropathy. We investigated whether leptin induced monocyte chemo- tactic peptide-1 (MCP-1) synthesis through the mitogen-activated protein kinase (MAPK) pathway using cultured VSMCs. Results: Plasma leptin concentrations were significantly higher in the diabetic group than in the controls. Plasma leptin levels were positively correlated with body mass index, fasting and postprandial blood glucose, hemoglobin A1c, total cholesterol, urinary albumin excretion, high-sensitivity C-reactive protein (hsCRP), and MCP-1 plasma levels, and negatively correlated with creatinine clearance values. In cultured VSMCs, leptin increased MCP-1 production in a dose-dependent manner, and this stimulating effect of leptin on MCP-1 expression was reversed by the MAPK (MEK) inhibitor PD98059. In addition, leptin stimulated the phosphorylation of MEK, extracellular signal-regulated kinase, and E26-like transcription factor, which are components of the MAPK pathway. Conclusions: Overall, these findings suggest that activation of leptin synthesis may promote MCP-1 activation in a diabetic environment via the MAPK pathway in VSMCs and that it possibly contributes to the acceleration of atherosclerosis.