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      • 鹿茸 藥針 製劑가 힌쥐 腎臟 組織의 抗酸化 作用에 미치는 影響

        윤철호,정지천,신억섭 한국한의학연구원 1996 한국한의학연구원논문집 Vol.2 No.1

        Cervus elaphus for herb-acupuncture solution (CEHAS) was tested for the effects of free radical generating enzyme and lipid peroxidation in rat's kidney. In vitro, levels of lipid peroxide in tissues of kidney were proportionally decreased to concentration of extracts prepared from CEHAS. They were much more decreased, when lipid perocidation was inducesd with ferrous iron(Fe II). Also, enzyme activities of xanthine oxidase were decreased. The ratio of type conversion of zanthine oxidase was lowered, too. But, it was not seen changes on enzyme activities of aldehyde oxidase. These results suggest that CEHAS decrease the activities of free radical generating enzymes such as xanthine oxidase which form lipid peroxide.

      • 全蝎 抽出物의 抗癲癎效果에 關한 硏究

        신현철,윤철호,김종대,정지천,신억섭,허근 한국한의학연구원 1997 한국한의학연구원논문집 Vol.3 No.1

        In convulsion state by PTZ in rat, anticonvulsive effect and some γ-aminobutyric acid (GABA)-related mechanisms of Bythus extract in brain was experimented. It was ingibited GABA-T activity, lipid peroxide generation and xanthine oxidase activity as scheduled administration in vitro and vivo. And the content of brain gutathione was increased as scheduled administration in rat. In convulsion state by PTZ of previously managed rat by Buthus extract, onset eime and duration were non-specific changes but recovery time and severity was remarkably reduced. In conclusion speculated that Buthus extract inhibits convulsion by control of GABA content in brain.

      • KCI등재후보

        Monocyte Chemoattractant Protein-1[MCP1] -2518 유전자 다형성과 주요 우울장애

        배치운,이지현,신윤경,김태석,김정진,이창욱,이수정,전태연,이철,백인호 大韓神經精神醫學會 2004 신경정신의학 Vol.43 No.4

        Object : This study was designed to examine the association between monocyte chemoattractant protein-l (MCPl) -2518poly morphism and major depressive disorder (MDD). Methods : Ninety patients with MDD and 114 healthy controls participated in this study. Genotyping was performed by the polymerase chain reaction-restriction fragment length polymorphism method. Results : Genotype and allele distributions in patients with MDD were significantly different from those of the controls, In particular, subjects with the allele A were found to have an increased risk of MDD. Conclusion : The present study suggests that the MCPl -2518 polymorphism may have a potential role for susceptibility to MDD in the Korean population and thus calls for consecutive studies in order to pile up the data with larger different ethnic background.

      • KCI등재후보

        실내사무환경의 환경성담배연기(ETS)의 지표물질에 관한 연구

        하권철,백남원,박동욱,윤충식,김원,최상준,박지영,최인자,김신범,강태선 한국산업위생학회 2003 한국산업보건학회지 Vol.13 No.2

        The purpose of this research is to evaluate indoor office environment using the concentrations of nicotine, 3-enthenyl-pyridine(3-EP), and respirable suspended particulate(RSP), which are indicators for environmental tobacco smoke(ETS) and the correlations between indicators and environmental conditions(smoking density, smoking index). The mean air charge per hour (ACH) in smoking rooms was 10.4 and most of the smoking rooms showed non-compliance withe ASHRAE standard value except only one smoking rooms. The concentrations of RSP, 3-EP, nicotine showed log=normal distributions, and became different statistically depending on smoking condition(p〈0.01). The geometric mean concentration of RSP in smoking room was 441.7 ug/㎡ that is far exceeded environmental standard(150 ug/㎡). This implies that fine particulate in smoking room should be carefully controlled considering smoking density and ventilation fate. The mean concentrations of nicotine and 3-EP were 93.4 ug/㎥, respectively. The correlation coefficients between RSP and SI, 3-EP and SI, and Nicotine and SI were 0.67, 0.84 and 0.74, respectively. The correlation coefficient between nicotine and 3-EP, nicotine and RSP, and RSP and 3-EP were 0.76,0.78 and 0.57 respectively.

      • KCI등재

        Remifentanil promotes osteoblastogenesis by upregulating Runx2/osterix expression in preosteoblastic C2C12 cells

        Yoon, Ji-Young,Kim, Tae-Sung,Ahn, Ji-Hye,Yoon, Ji-Uk,Kim, Hyung-Joon,Kim, Eun-Jung The Korean Dental Society of Anesthsiology 2019 Journal of Dental Anesthesia and Pain Medicine Vol.19 No.2

        Background: The imbalance between osteoblasts and osteoclasts can lead to pathological conditions such as osteoporosis. It has been reported that opioid adversely affect the skeletal system, but it is inconsistent. Remifentanil is currently used as an adjuvant analgesic drug in general anesthesia and sedation. The aim of the present study was to investigate the effect of remifentanil on the osteoblast differentiation and mechanism involved in this effect. Methods: The C2C12 cells (mouse pluripotent mesenchymal cell line) were used as preosteoblast. Osteoblastic differentiation potency was determined by alkaline phosphatase (ALP) staining. C2C12 cell migration by remifentanil was evaluated using Boyden chamber migration assay. The expression of Runx2 and osterix was evaluated by RT-PCT and western blot analysis to investigate the mechanism involved in remifentanil-mediated osteoblast differentiation. Results: ALP staining showed that remifentanil increased significantly osteoblast differentiation. In Boyden chamber migration assay, C2C12 cell migration was increased by remifentanil. RT-PCR and western blot analysis showed that the expression of Runx2 and osterix was upregulated by remifentanil. Conclusions: We demonstrated that remifentanil increased osteoblast differentiation in vitro by upregulation of Runx2 and osterix expression. Therefore, remifentanil has the potential for assisting with bone formation and bone healing.

      • KCI등재

        Dexmedetomidine attenuates H<sub>2</sub>O<sub>2</sub>-induced cell death in human osteoblasts

        Yoon, Ji-Young,Park, Jeong-Hoon,Kim, Eun-Jung,Park, Bong-Soo,Yoon, Ji-Uk,Shin, Sang-Wook,Kim, Do-Wan The Korean Dental Society of Anesthsiology 2016 Journal of Dental Anesthesia and Pain Medicine Vol.16 No.4

        Background: Reactive oxygen species play critical roles in homeostasis and cell signaling. Dexmedetomidine, a specific agonist of the ${\alpha}2$-adrenoceptor, has been commonly used for sedation, and it has been reported to have a protective effect against oxidative stress. In this study, we investigated whether dexmedetomidine has a protective effect against $H_2O_2$-induced oxidative stress and the mechanism of $H_2O_2$-induced cell death in normal human fetal osteoblast (hFOB) cells. Methods: Cells were divided into three groups: control group-cells were incubated in normoxia without dexmedetomidine, hydrogen peroxide ($H_2O_2$) group-cells were exposed to $H_2O_2$ ($200{\mu}M$) for 2 h, and Dex/$H_2O_2$ group-cells were pretreated with dexmedetomidine ($5{\mu}M$) for 2 h then exposed to $H_2O_2$ ($200{\mu}M$) for 2 h. Cell viability and apoptosis were evaluated. Osteoblast maturation was determined by assaying bone nodular mineralization. Expression levels of bone-related proteins were determined by western blot. Results: Cell viability was significantly decreased in the $H_2O_2$ group compared with the control group, and this effect was improved by dexmedetomidine. The Hoechst 33342 and Annexin-V FITC/PI staining revealed that dexmedetomidine effectively decreased $H_2O_2$-induced hFOB cell apoptosis. Dexmedetomidine enhanced the mineralization of hFOB cells when compared to the $H_2O_2$ group. In western blot analysis, bone-related protein was increased in the Dex/$H_2O_2$ group. Conclusions: We demonstrated the potential therapeutic value of dexmedetomidine in $H_2O_2$-induced oxidative stress by inhibiting apoptosis and enhancing osteoblast activity. Additionally, the current investigation could be evidence to support the antioxidant potential of dexmedetomidine in vitro.

      • KCI등재

        Propofol protects human keratinocytes from oxidative stress via autophagy expression

        Yoon, Ji-Young,Jeon, Hyun-Ook,Kim, Eun-Jung,Kim, Cheul-Hong,Yoon, Ji-Uk,Park, Bong-Soo,Yu, Su-Bin,Kwak, Jin-Won The Korean Dental Society of Anesthsiology 2017 Journal of Dental Anesthesia and Pain Medicine Vol.17 No.1

        Background: The skin consists of tightly connected keratinocytes, and prevents extensive water loss while simultaneously protecting against the entry of microbial pathogens. Excessive cellular levels of reactive oxygen species can induce cell apoptosis and also damage skin integrity. Propofol (2,6-diisopropylphenol) has antioxidant properties. In this study, we investigated how propofol influences intracellular autophagy and apoptotic cell death induced by oxidative stress in human keratinocytes. Method: The following groups were used for experimentation: control, cells were incubated under normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) without propofol; hydrogen peroxide ($H_2O_2$), cells were exposed to $H_2O_2$ ($300{\mu}M$) for 2 h; propofol preconditioning (PPC)/$H_2O_2$, cells pretreated with propofol ($100{\mu}M$) for 2 h were exposed to $H_2O_2$; and 3-methyladenine $(3-MA)/PPC/H_2O_2$, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to $H_2O_2$. Cell viability, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis. Results: Cell viability decreased significantly in the $H_2O_2$ group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased $H_2O_2$-induced cell apoptosis and increased cell migration. However, pretreatment with 3-MA inhibited the protective effect of propofol on cell apoptosis. Autophagy was activated in the $PPC/H_2O_2$ group compared to that in the $H_2O_2$ group as demonstrated by western blot analysis and autophagosome staining. Conclusion: The results suggest that propofol preconditioning induces an endogenous cellular protective effect in human keratinocytes against oxidative stress through the activation of signaling pathways related to autophagy.

      • KCI등재

        Optimal effect-site concentration of remifentanil to prevent hemodynamic changes during nasotracheal intubation using a video laryngoscope

        Yoon, Ji-Young,Park, Chul-Gue,Kim, Eun-Jung,Choi, Byung-Moon,Yoon, Ji-Uk,Kim, Yeon Ha,Lee, Moon Ok,Han, Ki Seob,Ahn, Ji-Hye The Korean Dental Society of Anesthsiology 2020 Journal of Dental Anesthesia and Pain Medicine Vol.20 No.4

        Background: Nasotracheal intubation is the most commonly used method to secure the field of view when performing surgery on the oral cavity or neck. Like orotracheal intubation, nasotracheal intubation uses a laryngoscope. Hemodynamic change occurs due to the stimulation of the sympathetic nervous system. Recently, video laryngoscope with a camera attached to the end of the direct laryngoscope blade has been used to minimize this change. In this study, we investigated the optimal effect-site concentration (Ce) of remifentanil for minimizing hemodynamic responses during nasotracheal intubation with a video laryngoscope. Methods: Twenty-one patients, aged between 19 and 60 years old, scheduled for elective surgery were included in this study. Anesthesia was induced by slowly injecting propofol. At the same time, remifentanil infusion was initiated at 3.0 ng/ml via target-controlled infusion (TCI). When remifentanil attained the preset Ce, nasotracheal intubation was performed using a video laryngoscope. The patient's blood pressure and heart rate were checked pre-induction, right before and after intubation, and 1 min after intubation. Hemodynamic stability was defined as an increase in systolic blood pressure and heart rate by 20% before and after nasotracheal intubation. The response of each patient determined the Ce of remifentanil for the next patient at an interval of 0.3 ng/ml. Results: The Ce of remifentanil administered ranged from 2.4 to 3.6 ng/ml for the patients evaluated. The estimated optimal effective effect-site concentrations of remifentanil were 3.22 and 4.25 ng/ml, that were associated with a 50% and 95% probability of maintaining hemodynamic stability, respectively. Conclusion: Nasotracheal intubation using a video laryngoscope can be successfully performed in a hemodynamically stable state by using the optimal remifentanil effect-site concentration (Ce<sub>50</sub>, 3.22 ng/ml; Ce<sub>95</sub>, 4.25 ng/ml).

      • KCI등재

        Propofol protects against oxidative-stress-induced COS-7 cell apoptosis by inducing autophagy

        Yoon, Ji-Young,Baek, Chul-Woo,Kim, Eun-Jung,Park, Bong-Soo,Yu, Su-Bin,Yoon, Ji-Uk,Kim, Eok-Nyun The Korean Dental Society of Anesthsiology 2017 Journal of Dental Anesthesia and Pain Medicine Vol.17 No.1

        Background: In oxidative stress, reactive oxygen species (ROS) production contributes to cellular dysfunction and initiates the apoptotic cascade. Autophagy is considered the mechanism that decreases ROS concentration and oxidative damage. Propofol shows antioxidant properties, but the mechanisms underlying the effect of propofol preconditioning (PPC) on oxidative injury remain unclear. Therefore, we investigated whether PPC protects against cell damage from hydrogen peroxide ($H_2O_2$)-induced oxidative stress and influences cellular autophagy. Method: COS-7 cells were randomly divided into the following groups: control, cells were incubated in normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) for 24 h without propofol; $H_2O_2$, cells were exposed to $H_2O_2$ ($400{\mu}M$) for 2 h; $PPC+H_2O_2$, cells pretreated with propofol were exposed to $H_2O_2$; and 3-methyladenine $(3-MA)+PPC+H_2O_2$, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to $H_2O_2$. Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) reduction. Apoptosis was determined using Hoechst 33342 staining and fluorescence microscopy. The relationship between PPC and autophagy was detected using western blot analysis. Results: Cell viability decreased more significantly in the $H_2O_2$ group than in the control group, but it was improved by PPC ($100{\mu}M$). Pretreatment with propofol effectively decreased $H_2O_2$-induced COS-7 cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol during apoptosis. Western blot analysis showed that the level of autophagy-related proteins was higher in the $PPC+H_2O_2$ group than that in the $H_2O_2$ group. Conclusion: PPC has a protective effect on $H_2O_2$-induced COS-7 cell apoptosis, which is mediated by autophagy activation.

      • KCI등재

        Protective effects of remifentanil against H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in human osteoblasts

        Yoon, Ji-Young,Kim, Do-Wan,Kim, Eun-Jung,Park, Bong-Soo,Yoon, Ji-Uk,Kim, Hyung-Joon,Park, Jeong-Hoon The Korean Dental Society of Anesthsiology 2016 Journal of Dental Anesthesia and Pain Medicine Vol.16 No.4

        Background: Bone injury is common in many clinical situations, such as surgery or trauma. During surgery, excessive reactive oxygen species (ROS) production decreases the quality and quantity of osteoblasts. Remifentanil decreases ROS production, reducing oxidative stress and the inflammatory response. We investigated remifentanil's protective effects against $H_2O_2$-induced oxidative stress in osteoblasts. Methods: To investigate the effect of remifentanil on human fetal osteoblast (hFOB) cells, the cells were incubated with 1 ng/ml of remifentanil for 2 h before exposure to $H_2O_2$. For induction of oxidative stress, hFOB cells were then treated with $200{\mu}M$ $H_2O_2$ for 2 h. To evaluate the effect on autophagy, a separate group of cells were incubated with 1 mM 3-methyladenine (3-MA) before treatment with remifentanil and $H_2O_2$. Cell viability and apoptotic cell death were determined via MTT assay and Hoechst staining, respectively. Mineralized matrix formation was visualized using alizarin red S staining. Western blot analysis was used to determine the expression levels of bone-related genes. Results: Cell viability and mineralized matrix formation increased on remifentanil pretreatment before exposure to $H_2O_2$-induced oxidative stress. As determined via western blot analysis, remifentanil pretreatment increased the expression of bone-related genes (Col I, BMP-2, osterix, and $TGF-{\beta}$). However, pretreatment with 3-MA before exposure to remifentanil and $H_2O_2$ inhibited remifentanil's protective effects on hFOB cells during oxidative stress. Conclusions: We showed that remifentanil prevents oxidative damage in hFOB cells via a mechanism that may be highly related to autophagy. Further clinical studies are required to investigate its potential as a therapeutic agent.

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