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Cho, Yong-Jun,Lee, Chi Hern,Kim, Dae Won,Yoo, Ki-Yeon,Eum, Won Sik,Shin, Min Jea,Jo, Hyo Sang,Park, Jinseu,Han, Kyu Hyung,Lee, Keun Wook,Choi, Soo Young Journal of Neurosurgery Publishing Group 2018 Journal of Neurosurgery: Spine Vol.29 No.5
<B>OBJECTIVE</B><P>Adhesion formation is one of the most common complications following laminectomy. The efficiency of antiadhesive agents is required to prevent postsurgical adhesion. Therefore, the authors investigated the effects of silk solution against laminectomy-induced dural adhesion formation in a rat model.</P><B>METHODS</B><P>The authors prepared the silk solution from silkworms. Laminectomies were performed between L3 and L5 in all rats. MediShield was used as a control. The effects of silk solution against laminectomy-induced dural adhesion formation and inflammation were confirmed by histological examination and Western blot analysis.</P><B>RESULTS</B><P>Laminectomy-induced dural adhesion formation was drastically reduced in silk solution-treated rats (Grade 2) compared to vehicle-treated rats (Grade 3). Dural adhesion formation was significantly reduced in rats that received treatment with silk solution or MediShield, which is a known antiadhesion drug. In addition, combined treatment with silk solution and MediShield showed greater reductions in inflammation compared to the silk solution- or MediShield-treated rats (p > 0.05).</P><B>CONCLUSIONS</B><P>In this study, the authors demonstrated that silk solution effectively reduced postlaminectomy dural adhesion formation in rats. Although further studies on the long-term effects are necessary to validate these results, silk solution may potentially serve as an antiadhesion agent in neurological procedures.</P>
Eum, Won Sik,Shin, Min Jea,Lee, Chi Hern,Yeo, Hyeon Ji,Yeo, Eun Ji,Choi, Yeon Joo,Kwon, Hyun Jung,Kim, Duk-Soo,Kwon, Oh Shin,Lee, Keun Wook,Han, Kyu Hyung,Park, Jinseu,Kim, Dae Won,Choi, Soo Young Elsevier 2019 Biochimie Vol.156 No.-
<P><B>Abstract</B></P> <P>Parkinson's disease (PD), a neurodegenerative disorder, is characterized by a loss of dopaminergic neurons in the substantia nigra (SN) of the brain and it is well known that the pathogenesis of PD is related to a number of risk factors including oxidative stress. Antioxidant 1 (ATOX1) protein plays a crucial role in various diseases as an antioxidant and chaperone. In this study, we determined whether Tat-ATOX1 could protect against 1-methyl-4-phenylpyridinium ion (MPP<SUP>+</SUP>)-induced SH-SY5Y cell death and in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced animal model of PD. In the MPP<SUP>+</SUP> exposed SH-SY5Y cells, Tat-ATOX1 markedly inhibited cell death and toxicities. In addition, Tat-ATOX1 markedly suppressed the activation of Akt and mitogen activated protein kinases (MAPKs) as well as cleavage of caspase-3 and Bax expression levels. In a MPTP-induced animal model, Tat-ATOX1 transduced into brain and protected dopaminergic neuronal cell loss. Taken together, Tat-ATOX1 inhibits dopaminergic neuronal death through the suppression of MAPKs and apoptotic signal pathways. Thus, Tat-ATOX1 represents a potential therapeutic protein drug candidate for PD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Tat-ATOX1 transduces into SH-SY5Y cells and inhibited MPP<SUP>+</SUP>-induced cell death. </LI> <LI> Tat-ATOX1 suppressed the activation of Akt and MAPKs in MPP<SUP>+</SUP> exposed SH-SY5Y cells. </LI> <LI> Tat-ATOX1 inhibited dopaminergic neuronal cell loss in MPTP-induced animal model. </LI> <LI> Tat-ATOX1 represent a potential therapeutic agent for PD. </LI> </UL> </P>
( Dae Won Kim ),( Sung Ho Lee ),( Min Jea Shin ),( Kibom Kim ),( Sae Kwang Ku ),( Jong Kyu Youn ),( Su Bin Cho ),( Jung Hwan Park ),( Chi Hern Lee ),( Ora Son ),( Eun Jeong Sohn ),( Sung Woo Cho ),( J 생화학분자생물학회(구 한국생화학분자생물학회) 2015 BMB Reports Vol.48 No.11
FK506 binding protein 12 (FK506BP) is a small peptide with a single FK506BP domain that is involved in suppression of immune response and reactive oxygen species. FK506BP has emerged as a potential drug target for several inflammatory diseases. Here, we examined the protective effects of directly applied cell permeable FK506BP (PEP-1-FK506BP) on corneal alkali burn injury (CAI). In the cornea, there was a significant decrease in the number of cells expressing pro-inflammation, apoptotic, and angiogenic factors such as TNF-, COX-2, and VEGF. Both corneal opacity and corneal neovascularization (CNV) were significantly decreased in the PEP-1-FK506BP treated group. Our results showed that PEP-1-FK506BP can significantly inhibit alkali burn-induced corneal inflammation in rats, possibly by accelerating corneal wound healing and by reducing the production of angiogenic factors and inflammatory cytokines. These results suggest that PEP-1-FK506BP may be a potential therapeutic agent for CAI. [BMB Reports 2015; 48(11): 618-623]
Protective effects of Tat-DJ-1 protein against streptozotocin-induced diabetes in a mice model
( Hyeon Ji Yeo ),( Eun Ji Yeo ),( Min Jea Shin ),( Yeon Joo Choi ),( Chi Hern Lee ),( Hyeok Yil Kwon ),( Dae Won Kim ),( Won Sik Eum ),( Soo Young Choi ) 생화학분자생물학회(구 한국생화학분자생물학회) 2018 BMB Reports Vol.51 No.7
A major feature of type 1 diabetes mellitus (T1DM) is hyperglycemia and dysfunction of pancreatic β-cells. In a previous study, we have shown that Tat-DJ-1 protein inhibits pancreatic RINm5F β-cell death caused by oxidative stress. In this study, we examined effects of Tat-DJ-1 protein on streptozotocin (STZ)-induced diabetic mice. Wild type (WT) Tat-DJ-1 protein transduced into pancreas where it markedly inhibited pancreatic β-cell destruction and regulated levels of serum parameters including insulin, alkaline phosphatase (ALP), and free fatty acid (FFA) secretion. In addition, transduced WT Tat-DJ-1 protein significantly inhibited the activation of NF-kB and MAPK (ERK and p38) expression as well as expression of COX-2 and iNOS in STZ exposed pancreas. In contrast, treatment with C106A mutant Tat-DJ-1 protein showed no protective effects. Collectively, our results indicate that WT Tat-DJ-1 protein can significantly ameliorate pancreatic tissues in STZ-induced diabetes in mice. [BMB Reports 2018; 51(7): 362-367]
위절제술이 골대사 및 골밀도에 미치는 영향 - 예검법으로서 의미있는 지표
권성준(Sung Joon Kwon),신동일(Donng Ill Shin),원치규(Chi Kyooh Won),전규영(Kyu Young Jun),곽진영(Jin Young Kwak),이광수(Kwang Soo Lee),정파종(Pa Jong Jung),안유헌(Yoo Hern Ahn),함준수(Joon Soo Hahm),김목현(Mok Hyun Kim) 대한소화기학회 1996 대한소화기학회지 Vol.28 No.2
N/A Background/Aims: Abnormalities of bone metabolism occur to gastrectomised patients in the form of a late complication. Nowadays, many biochemical and radiologic measurements are applied to detect these abnormalities. The aim of this study was to determine the parameter for an appropriate screening test during the long-term follow-up period and define the usefulness of new biochemical markers for bone metabo]ism by comparing them with traditional markers. Methods: Among the patients gastrectomised(Billroth II) in the surgica] department of Hanyang University Hospital since 1982, 10 patients were randomly selected with exclusion criteria by measuring several biochemical and radiologic tests. Ten age-matched volunteers who led a healthy normal life were selected with the consent of subjects. Results: Comparing the data with those of a corresponding control group, the ]umbar bone density tneasured by quantitative cornputed tornography(QCT) was statistically significantly lower in the patient group(p0.01). In addition, urinary deoxypyridinoline (DPD), a biochemical marker for bone resorption, was statistica]ly higher in the patient group(p -0.025). Osteocalcin, P1CP, and 1CTP were slightly but not significant]y bigher in the patient group. The serum PTH and 25-hydroxyvitamin D levels were sitnilar in both groups. Conclusiions: Although the nurnber of cases was smal] for data evaluation, we suggest that urinary deoxypyridinoline and QCT were appropriate parameters for tbe screening test for the detection of bone metabolism abnormalities in gastrectomised patients during the long-term follow-up. Furthermore, urinary deoxypyridinoline is a simple and rapid test which can replace cumbersome 24-hour urinary hydroxypro]ine. (Korean J Gastroenterol 1996; 28:172 178)
Transduced Tat-DJ-1 protein inhibits cytokines-induced pancreatic RINm5F cell death
( Hyo Sang Jo ),( Hyeon Ji Yeo ),( Hyun Ju Cha ),( Sang Jin Kim ),( Su Bin Cho ),( Jung Hwan Park ),( Chi Hern Lee ),( Eun Ji Yeo ),( Yeon Joo Choi ),( Won Sik Eum ),( Soo Young Choi ) 생화학분자생물학회(구 한국생화학분자생물학회) 2016 BMB Reports Vol.49 No.5
Loss of pancreatic β-cells by oxidative stress or cytokines is associated with diabetes mellitus (DM). DJ-1 is known to as a multifunctional protein, which plays an important role in cell survival. We prepared cell permeable wild type (WT) and mutant type (M26I) Tat-DJ-1 proteins to investigate the effects of DJ-1 against combined cytokines (IL-1β, IFN-γ and TNF-α)-induced RINm5F cell death. Both Tat-DJ-1 proteins were transduced into RINm5F cells. WT Tat-DJ-1 proteins significantly protected against cell death from cytokines by reducing intracellular toxicities. Also, WT Tat-DJ-1 proteins markedly regulated cytokines-induced pro- and anti-apoptosis proteins. However, M26I Tat-DJ-1 protein showed relatively low protective effects, as compared to WT Tat-DJ-1 protein. Our experiments demonstrated that WT Tat-DJ-1 protein protects against cytokine-induced RINm5F cell death by suppressing intracellular toxicities and regulating apoptosisrelated protein expression. Thus, WT Tat-DJ-1 protein could potentially serve as a therapeutic agent for DM and cytokine related diseases. [BMB Reports 2016; 49(5): 297-302]
Jo, Hyo Sang,Cha, Hyun Ju,Kim, Sang Jin,Yeo, Hyeon Ji,Cho, Su Bin,Park, Jung Hwan,Lee, Chi Hern,Yeo, Eun Ji,Choi, Yeon Joo,Eum, Won Sik,Choi, Soo Young Springer US 2016 MEDICINAL CHEMISTRY RESEARCH Vol.25 No.11
<P>Oxidative stress is highly involved in the development of diabetes mellitus by destruction of pancreatic β-cells. DJ-1 is an antioxidant protein and DJ-1 expression levels are known to be reduced in diabetes mellitus. Thus, we examined the effects of DJ-1 protein against oxidative stress-induced pancreatic β-cell (RINm5F) death using cell permeable wild-type and mutant-type (C106A) Tat-DJ-1 proteins, which both efficiently transduced into RINm5F cells. Intracellular stability of wild-type Tat-DJ-1 persisted two times longer than C106A Tat-DJ-1. Wild-type Tat-DJ-1 protein markedly protected cells from hydrogen peroxide-induced toxicities such as cell death, reactive oxygen species generation, and DNA fragmentation. Further, wild-type Tat-DJ-1 protein significantly inhibited hydrogen peroxide-induced activation of mitogen-activated protein kinases and NF-κB signaling. On the other hand, C106A Tat-DJ-1 protein did not show the same protective effects. These results indicate that wild-type Tat-DJ-1 inhibits oxidative stress-induced cellular toxicity and activation of mitogen-activated protein kinases and NF-κB signals in RINm5F cells. These results suggest that wild-type Tat-DJ-1 protein may be a potential therapeutic agent against diabetes mellitus or toward the prevention of pancreatic β-cell destruction.</P>
Transduced Tat-DJ-1 protein inhibits cytokines-induced pancreatic RINm5F cell death
( Hyo Sang Jo ),( Hyeon Ji Yeo ),( Hyun Ju Cha ),( Sang Jin Kim ),( Su Bin Cho ),( Jung Hwan Park ),( Chi Hern Lee ),( Eun Ji Yeo ),( Yeon Joo Choi ),( Won Sik Eum ),( Soo Young Choi ) 생화학분자생물학회(구 한국생화학분자생물학회) 2016 BMB Reports Vol.49 No.6
Loss of pancreatic β-cells by oxidative stress or cytokines is associated with diabetes mellitus (DM). DJ-1 is known to as a multifunctional protein, which plays an important role in cell survival. We prepared cell permeable wild type (WT) and mutant type (M26I) Tat-DJ-1 proteins to investigate the effects of DJ-1 against combined cytokines (IL-1β, IFN-Υ and TNF-α)-induced RINm5F cell death. Both Tat-DJ-1 proteins were transduced into RINm5F cells. WT Tat-DJ-1 proteins significantly protected against cell death from cytokines by reducing intracellular toxicities. Also, WT Tat-DJ-1 proteins markedly regulated cytokines-induced pro- and anti-apoptosis proteins. However, M26I Tat-DJ-1 protein showed relatively low protective effects, as compared to WT Tat-DJ-1 protein. Our experiments demonstrated that WT Tat-DJ-1 protein protects against cytokine-induced RINm5F cell death by suppressing intracellular toxicities and regulating apoptosisrelated protein expression. Thus, WT Tat-DJ-1 protein could potentially serve as a therapeutic agent for DM and cytokine related diseases. [BMB Reports 2016; 49(5): 297-302]