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

In vivo Electron Spin Resonance: An Effective New Tool for Reactive Oxygen Species/Reactive Nitrogen Species Measurement

Jin Yi Han,홍진태,오기완 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.9

Reactive oxygen species are regarded as important factors in the initiation and progression of many diseases. Therefore, measurement of redox status would be helpful in understanding the “Redox Navigation” of such diseases. Because electron spin resonance (ESR) shows good signal responses to nitroxyl radical and various redox-related species, such as oxygen radicals and antioxidants, the in vivo ESR/nitroxyl probe technique can provide useful information on real-time redox status in a living body. ESR spectrometers for in vivo measurements can be operated at lower frequencies (approximately 3.5 GHz, 1 GHz, 700 MHz, and 300 MHz) than usual (9-10 GHz). Several types of resonators were also designed to minimize the dielectric loss of electromagnetic waves caused by water in animal bodies. In vivo ESR spectroscopy and its imaging have been used to analyze radical generation, redox status, partial pressure of oxygen and other conditions in various diseases. In addition, ESR has been used to analyze injury models related to oxidative stresses, such as nitroxyl radicals. The application of in vivo ESR for diseases related to oxidative injuries currently being investigated and the accumulation of basic data for therapy is ongoing. Recent progress in the instrumentation for in vivo ESR spectroscopy and its application to the life sciences are reviewed, because measurement of redox status in vivo is considered necessary to understand the initiation and progression of diseases.

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

Jin-Yi Han,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.

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.

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.

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>