http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Bupivacaine과 ropivacaine이 Xenopus oocyte에 발현된 HERG 전류에 미치는 영향
김국성,이규승,김효신,손숙진,이상도,김광진,전병화,김윤희,박진봉 충남대학교 의과대학 의학연구소 2003 충남의대잡지 Vol.30 No.1
Bupivacaine is an amide-type local anesthetic widely used for regional anesthesia. Ropivacaine is developed as a less cardiotoxic alternatives to bupivacaine. In the present study, we have analyzed the effects of bupivacaine and ropivacaine on HERG currents expressed in Xenopus oocytes. Bupivacaine and ropivacaine(3∼1,000μM) blocked HERG currents in a concentration dependent manner. EC_(50) was 26.1±3.1μM(n_(R) 0.65±0.04) and 43.5±7.9μM(n_(H) 0.99±0.13) in bupivacaine and ropivacaine, respectively. Bupivacaine and ropivacaine did not affect the activation and deactivation kinetics of HERG channels. However, the drugs decreased the slope conductance measured from fully activated current-voltage relationship curves. These results suggest that bupivacaine and ropivacaine have a similarinhibitory effect on HERG channels, which could be a possible cellular mechanism of LQT or ventricular arrythmia by the drugs.
Analysis of Blood Flow-dependent Blood Nitric Oxide Level and Half-life of Nitric Oxide in Vivo
Kim Cuk-Seong,Kim Hyo-Shin,Lee Young-Jun,Park Jin Bory,Ryoo Sung-Woo,Chang Seok-Jang,Jeon Byeong-Hwa Biomedical Engineering Society for Circulation 2003 International Journal of Vascular Biomedical Engin Vol.1 No.2
Endothelial release of nitric oxide (NO) contributes to the regulation of vascular tone by inducing vascular relaxation. To estimate the blood flow-dependent nitric oxide level and half-life (T1/2) of nitric oxide in vivo state, we investigated the change of aortic NO currents during the change of aortic blood flow rate using NO-selective electrode system and electromagnetic flowmeter in the aorta of anesthetized rats. Resting mean aortic blood flow rate was $49.6{\pm}5.6ml/min$ in the anesthetized rats. NO currents in the aorta were increased by the elevation of blood pressure and/or blood flow rate. When the aortic blood flow was occluded by the clamping, aortic NO currents were decreased. The difference of NO concentration between resting state and occluded state was $1.34{\pm}0.26{\mu}M$ (n=7). This NO concentration was estimated as blood flow-dependent nitric oxide concentration in the rats. Also, while the aortic blood flow was occluded, NO currents were decreased with exponential pattern with $12.84{\pm}2.15$ seconds of time constant and $7.70{\pm}1.07$ seconds of half-life. To summarize, this study suggested that blood flow-dependent NO concentration and half-life of nitric oxide were about $1.3{\mu}M$ and 7.7 seconds, respectively, in the aorta of anesthetized rats. The nitric oxide-selective electrode system is useful for the direct and continuous measurement of NO in vivo state.
P53 Impairs Endothelium-Dependent Vasomotor Function Through Transcriptional Upregulation of P66shc
Kim, Cuk-Seong,Jung, Saet-Byel,Naqvi, Asma,Hoffman, Timothy A.,DeRicco, Jeremy,Yamamori, Tohru,Cole, Marsha P.,Jeon, Byeong-Hwa,Irani, Kaikobad Ovid Technologies Wolters Kluwer -American Heart A 2008 Circulation research Vol.103 No.12
<P>The transcription factor, p53, and the adaptor protein, p66shc, both play essential roles in promoting oxidative stress in the vascular system. However, the relationship between the two in the context of endothelium-dependent vascular tone is unknown. Here, we report a novel, evolutionarily conserved, p53-mediated transcriptional mechanism that regulates p66shc expression and identify p53 as an important determinant of endothelium-dependent vasomotor function. We provide evidence of a p53 response element in the promoter of p66shc and show that angiotensin II-induced upregulation of p66shc in endothelial cells is dependent on p53. In addition, we demonstrate that downregulation of p66shc expression, as well as inhibition of p53 function in mice, mitigates angiotensin II-induced impairment of endothelium-dependent vasorelaxation, decrease in bioavailable nitric oxide, and hypertension. These findings reveal a novel p53-dependent transcriptional mechanism for the regulation of p66shc expression that is operative in the vascular endothelium and suggest that this mechanism is important in impairing endothelium-dependent vascular relaxation.</P>
백서의 피부 및 뇌혈류에 미치는 고려홍삼 사포닌 및 비사포닌의 영향
김신희(Shin Hee Kim),김국성(Cuk Seong Kim),박진봉(Jin Bong Park),한찬수(Chan Soo Han),김광진(Kwang-Jin Kim),김신혜(Shin Hye Kim),김세훈(Se Hoon Kim),남기열(Ki Yeul Nam),전병화(Byeong Hwa Jeon) 고려인삼학회 2002 Journal of Ginseng Research Vol.26 No.3
본 연구에서는 혈류량의 변화를 실시간으로 측정할 수 있는 레이져 도플러 혈류량측정장치를 이용하여 피부혈류 및 뇌혈류량에 미치는 고려홍삼의 사포닌과 비사포닌의 효능을 연구하고자 고려홍삼의 정맥내 복강내 및 구강내로 주입하고 혈류의 변화를 관찰하여 다음과 같은 결론을 얻었다. 고려 홍삼<br/> 의 사포닌 성분은 피부혈류량에는 영향을 주지 않으나 뇌혈류량을 증가시키는 효능이 있다. 고려 홍삼의 비사포닌 성분은 피부혈류량 및 뇌혈류량에 거의 영향을 주지 않았다. 고려홍삼 사포닌에 의한 뇌혈류량의 증가는 복강내 및 경구로 투여할 경우는 관찰할 수 있으나 정맥내로 직접 투여할 경우는<br/> 관찰되지 않았다.이상의결과를종합해볼때고려홍삼의 사포닌 성분은 뇌혈류량을 증가시키는 혈류개선작용이 있는 것으로 사료된다. To study the effect of Korea red ginseng (KRG) on the skin and cerebral blood flow, we evaluated the change of skin perfusion rate and cerebral perfusion rate after the intravenous, intraperitoneal, and oral administration of crude saponin (CS) and saponin-free fraction (SFF) of KRG in the rats. The change of skin perfusion rate and cerebral perfusion rate was measured laser doppler flowmetry. The intravenous injections of CS or SFF of KRG and intraperitoneal injection of SFF of KRG did not change the relative skin and cerebral blood flow in the rats. When the rats were treated by the<br/> intraperitoneal injection of CS of KRG, relative cerebral blood flow was significantly increased with a time-dependent manner, however, relative skin blood flow was not influenced by the them. Oral administration of CS of KRG slightly increased skin blood flow in the rats. Also, the change of cerebral blood flow by transient bilateral carotid arterial clamp in the CS-treated rats was significantly decreased, compared with control groups. From the above results, it was suggested that Korea red ginseng have a increasing property of cerebral blood flow in the rats.<br/> Key words : Korea Red Ginseng, Cerebral blood flow, Skin blood flow, Laser Doppler flowmeter.
Choi, Su-jeong,Piao, Shuyu,Nagar, Harsha,Jung, Saet-byel,Kim, Seonhee,Lee, Ikjun,Kim, Sung-min,Song, Hee-Jung,Shin, Nara,Kim, Dong Woon,Irani, Kaikobad,Jeon, Byeong Hwa,Park, Jeen-Woo,Kim, Cuk-Seong Elsevier 2018 Biochemical and biophysical research communication Vol.503 No.3
<P><B>Abstract</B></P> <P>Isocitrate dehydrogenase 2 (IDH2) is an essential enzyme in the mitochondrial antioxidant system, which produces nicotinamide adenine dinucleotide phosphate, and thereby defends against oxidative stress. We have shown that IDH2 downregulation results in mitochondrial dysfunction and reactive oxygen species (ROS) generation in mouse endothelial cells. The redox enzyme p66shc is a key factor in regulating the level of ROS in endothelial cells. In this study, we hypothesized that IDH2 knockdown-induced mitochondrial dysfunction stimulates endothelial inflammation, which might be regulated by p66shc-mediated oxidative stress. Our results showed that IDH2 downregulation led to mitochondrial dysfunction by decreasing the expression of mitochondrial oxidative phosphorylation complexes I, II, and IV, reducing oxygen consumption, and depolarizing mitochondrial membrane potential in human umbilical vein endothelial cells (HUVECs). The dysfunction not only increased mitochondrial ROS levels but also activated p66shc expression in HUVECs and IDH2 knockout mice. IDH2 deficiency increased intercellular adhesion molecule (ICAM)-1 expression and mRNA levels of pro-inflammatory cytokines (tumor necrosis factor [TNF]-α, and interleukin [IL]-1β) in HUVECs. The mRNA expression of ICAM-1 in endothelial cells and plasma levels of TNF-α and IL-1β were also markedly elevated in IDH2 knockout mice. However, p66shc knockdown rescued IDH2 deficiency-induced mitochondrial ROS levels, monocyte adhesion, ICAM-1, TNF-α, and IL-1β expression in HUVECs. These findings suggest that IDH2 deficiency induced endothelial inflammation via p66shc-mediated mitochondrial oxidative stress.</P> <P><B>Highlights</B></P> <P> <UL> <LI> IDH2 deficiency triggers severe mitochondrial dysfunction in HUVECs. </LI> <LI> IDH2 deficiency induces endothelial inflammation by the increased mitochondrial ROS and p66shc expression. </LI> <LI> p66shc mediated IDH2 deficiency-induced inflammatory molecule expression in HUVECs. </LI> </UL> </P>
Midazolam Inhibits Proinflammatory Mediators in the Lipopolysaccharide-activated Macrophage
Kim, Seon Nyo,Son, Soo Chang,Lee, Sang Mook,Kim, Cuk Seong,Yoo, Dae Goon,Lee, Sang Ki,Hur, Gang Min,Park, Jin Bong,Jeon, Byeong Hwa American Society of Anesthesiologists, Inc. 2006 Anesthesiology Vol.105 No.1
BACKGROUND:: Midazolam, a benzodiazepine, has a hypnotic effect and is widely used as a sedative. The role of midazolam in activation of macrophages during sepsis is not known. The aim of this study was to evaluate the antiinflammatory actions of midazolam in cultured macrophages. METHODS:: Using a macrophage cell line, RAW264.7 cells, the effect of midazolam on proinflammatory mediators and activation of mitogen-activated protein kinase was measured by Western blot. Nuclear factor-&kgr;B (NF-&kgr;B) activation and translocation of p65 subunit of NF-&kgr;B was measured using luciferase assay and immunocytochemistry. Superoxide production was measured by lucigenin chemiluminescence. RESULTS:: Midazolam significantly inhibited lipopolysaccharide-induced up-regulation of both cyclooxygenase 2 and inducible nitric oxide synthase in a dose-dependent manner (approximately 3–30 μm). I&kgr;B-α degradation and NF-&kgr;B transcriptional activity induced by lipopolysaccharide were also suppressed by the midazolam. Nuclear translocation of the p65 subunit of NF-&kgr;B was inhibited by midazolam. Furthermore, midazolam suppressed phosphorylation of p38 mitogen-activated protein kinase and also inhibited lipopolysaccharide-induced superoxide production in macrophages. CONCLUSIONS:: These results suggest that midazolam has an antiinflammatory action by inhibiting inducible nitric oxide synthase and cyclooxygenase-2 expression, possibly through suppression of NF-&kgr;B and p38 mitogen-activated protein kinase activation.