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Proteomic Analysis of Colonic Mucosal Tissue from Tuberculous and Ulcerative Colitis Patients
권성춘,원경종,Seoung Hyo Jung,이강파,Dong-Youb Lee,Eun-Seok Park,김보경,천갑진,한군희 대한약리학회 2012 The Korean Journal of Physiology & Pharmacology Vol.16 No.3
Changes in the expression profiles of specific proteins leads to serious human diseases, including colitis. The proteomic changes related to colitis and the differential expression between tuberculous (TC) and ulcerative colitis (UC) in colon tissue from colitis patients has not been defined. We therefore performed a proteomic analysis of human TC and UC mucosal tissue. Total protein was obtained from the colon mucosal tissue of normal, TC, and UC patients, and resolved by 2-dimensional electrophoresis (2-DE). The results were analyzed with PDQuest using silver staining. We used matrix-assisted laser desorption ionization time-of-flight/time-of-flight spectrometry (MALDI TOF/TOF) to identify proteins differentially expressed in TC and UC. Of the over 1,000 proteins isolated, three in TC tissue and two in UC tissue displayed altered expression when compared to normal tissue. Moreover, two proteins were differentially expressed in a comparative analysis between TC and UC. These were identified as mutant β-actin, α-enolase and Charcot-Leyden crystal protein. In particular, the expression of α- enolase was significantly greater in TC compared with normal tissue, but decreased in comparison to UC, implying that α-enolase may represent a biomarker for differential diagnosis of TC and UC. This study therefore provides a valuable resource for the molecular and diagnostic analysis of human colitis.
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기니 픽 장관 평활근에서 Sodium Nitroprusside가 장력에 미치는 영향
권성춘,김시연,김은주,강복순,Kwon, Seong-Chun,Kim, Si-Yeon,Kim, Eun-Ju,Kang, Bok-Soon 대한약리학회 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.6
Nitric oxide (NO) has been 3mown as a mediator of nonadrenergic, noncholinergic inhibitory neurotransmitter in intestinal smooth muscles. It has been suggested that NO donor such as sodium nitroprusside (SNP) produces relaxation of smooth muscle via activation of guanylate cyclase and elevation of cGMP levels. We have therefore investigated the effects of NO, using SNP, on muscle tension in the longitudinal smooth muscle of guinea-pig ileum. The possible role of cGMP was also investigated as well as the involvement of $K^+$ channel on SNP-induced inhibitory effect. The results are summarized as follows; high KCI-or CCh-activated contractions were inhibited by SNP in a concentration-dependent manner. 8-Br-cGMP also showed a similar effect in that of SNP TEA (1 mM) significantly reduced the SNP-induced inhibitory effect. SNP-induced effect was forther reduced by the presence of 10 mM TEA. On the other hand, 4-AP (0.1 mM), glibenclamide $(10\;{\mu}M)$ and apinain $(0.1\;{\mu}M)$ showed little effects on SNP-induced relaxation. Zaprinast significantly potentiated the SNP-induced inhibitory effect in all ranges. ODQ also significantly decreased the SNP-induced inhibitory effect. Pretreatment with CPA $(10\;{\mu}M)$ slightly reduced the SNP-induced inhibitory effect. From the above results, both effect mediated by NO and cGMP might be responsible for the activation of $Ca^{2+}$-activated $K^+$ channel by SNP in guinea-rig ileum. And this $K^+$ channel activation by SNP also contributes to the SNP-induced membrane hyperpolarization and relaxation.
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송용진,권성춘 대한약리학회 2004 The Korean Journal of Physiology & Pharmacology Vol.8 No.6
The present study were designed to characterize the action mechanisms of acetylcholine (ACh)- induced endothelium-dependent relaxation in arteries precontracted with high K+ (70 mM). For this, we simultaneously measured both muscle tension and cytosolic free Ca2+ concentration ([Ca2+]i), using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high K+ increased both [Ca2+]i and muscle tension whereas ACh (10μM) significantly relaxed the muscle and increased [Ca2+]i. In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased [Ca2+]i without relaxing the muscle. In the artery without endothelium, high K+ increased both [Ca2+]i and muscle tension although ACh was ineffective. 4-DAMP (10 nM) or atropine (0.1μM) abolished ACh-induced increase in [Ca2+]i and relaxation. The increase of [Ca2+]i and vasorelaxation by ACh was siginificantly reduced by either 3μM gadolinium, 10μM lanthanum, or by 10μM SKF 96365. These results suggest that in rabbit carotid artery, ACh-evoked relaxation of 70 mM K+-induced contractions appears to be mediated by the release of NO. ACh-evoked vasorelaxation is mediated via the M3 subtype, and activation of the M3 subtype is suggested to stimulate nonselective cation channels, leading to increase of [Ca2+]i in endothelial cells.
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옥성호,권성춘,강세빈,최문정,손주태 대한마취통증의학회 2014 Korean Journal of Anesthesiology Vol.67 No.6
Background: Mepivacaine induces contraction or decreased blood flow both in vivo and in vitro. Vasoconstriction is associatedwith an increase in the intracellular calcium concentration ([Ca2+]i). However, the mechanism responsible forthe mepivacaine-evoked [Ca2+]i increase remains to be determined. Therefore, the objective of this in vitro study was toexamine the mechanism responsible for the mepivacaine-evoked [Ca2+]i increment in isolated rat aorta. Methods: Isometric tension was measured in isolated rat aorta without endothelium. In addition, fura-2 loaded aorticmuscle strips were illuminated alternately (48 Hz) at two excitation wavelengths (340 and 380 nm). The ratio of F340 toF380 (F340/F380) was regarded as an amount of [Ca2+]i. We investigated the effects of nifedipine, 2-aminoethoxydiphenylborate(2-APB), gadolinium chloride hexahydrate (Gd3+), low calcium level and Krebs solution without calcium onthe mepivacaine-evoked contraction in isolated rat aorta and on the mepivacaine-evoked [Ca2+]i increment in fura-2loaded aortic strips. We assessed the effect of verapamil on the mepivacaine-evoked [Ca2+]i increment. Results: Mepivacaine produced vasoconstriction and increased [Ca2+]i. Nifedipine, 2-APB and low calcium attenuated vasoconstrictionand the [Ca2+]i increase evoked by mepivacaine. Verapamil attenuated the mepivacaine-induced [Ca2+]i increment. Calcium-free solution almost abolished mepivacaine-induced contraction and strongly attenuated the mepivacaineinduced[Ca2+]i increase. Gd3+ had no effect on either vasoconstriction or the [Ca2+]i increment evoked by mepivacaine. Conclusions: The mepivacaine-evoked [Ca2+]i increment, which contributes to mepivacaine-evoked contraction, appearsto be mediated mainly by calcium influx and partially by calcium released from the sarcoplasmic reticulum.
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옥성호,배성일,권성춘,박정철,김우찬,박경은,신일우,이헌근,정영균,최문정,손주태 대한통증학회 2014 The Korean Journal of Pain Vol.27 No.3
Background: A toxic dose of bupivacaine produces vasodilation in isolated aortas. The goal of this in vitro study was to investigate the cellular mechanism associated with bupivacaine-induced vasodilation in isolated endotheliumdenuded rat aortas precontracted with phenylephrine. Methods: Isolated endothelium-denuded rat aortas were suspended for isometric tension recordings. The effects of nifedipine, verapamil, iberiotoxin, 4-aminopyridine, barium chloride, and glibenclamide on bupivacaine concentration-response curves were assessed in endothelium-denuded aortas precontracted with phenylephrine. The effect of phenylephrine and KCl used for precontraction on bupivacaine-induced concentration-response curves was assessed. The effects of verapamil on phenylephrine concentration-response curves were assessed. The effects of bupivacaine on the intracellular calcium concentration ([Ca2+]i) and tension in aortas precontracted with phenylephrine were measured simultaneously with the acetoxymethyl ester of a fura-2-loaded aortic strip. Results: Pretreatment with potassium channel inhibitors had no effect on bupivacaine-induced relaxation in the endothelium-denuded aortas precontracted with phenylephrine, whereas verapamil or nifedipine attenuated bupivacaine-induced relaxation. The magnitude of the bupivacaine-induced relaxation was enhanced in the 100 mM KCl-induced precontracted aortas compared with the phenylephrine-induced precontracted aortas. Verapamil attenuated the phenylephrine-induced contraction. The magnitude of the bupivacaine-induced relaxation was higher than that of the bupivacaine-induced [Ca2+]i decrease in the aortas precontracted with phenylephrine.
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Mechanism of vasodilation by propofol in the rabbit renal artery
Seung Yong Park,정일,권성춘 대한마취통증의학회 2011 Anesthesia and pain medicine Vol.6 No.4
Background: Propofol directly inhibits vascular reactivity. However,available information regarding the underlying mechanisms of propofol is poor. Therefore, mechanisms of the underlying relaxant action of propofol were investigated using rabbit renal arteries. Methods: Propofol-induced relaxation of rabbit renal arteries was studied in contracted preparations with 50 mM KCl or 10 μM histamine. Vessel tension was recorded with a pen recorder. We were interested in determining whether propofol-induced vasodilation is affected by endothelium-denudation, L-NG-nitroarginine methyl ester (L-NAME), tetraethylammonium (TEA), iberiotoxin,glibenclamide, 4-aminopyridine, 7-ethoxyresorufin, caffeic acid,baiclalein, ryanodine, and thapsigargin. Results: Propofol-induced concentration-dependent vasodilation was not affected either by endothelium denudation or by L-NAME during histamine-induced contraction. The relaxing effect of propofol on histamine-induced contraction was inhibited by either TEA, a K+channel inhibitor, or iberiotoxin (100 nM), a selective blocker of the large conductance Ca2+-activated K+ channel (BKCa channel). In contrast, the relaxing effect of propofol was unaffected by 10 μM glibenclamide, an ATP-sensitive K+ channel blocker, by 5 mM 4-aminopyridine, a blocker of delayed rectifier, by 7-ethoxyresorufin,a cytochrome P450 inhibitor, by 10 μM caffeic acid and 10 μM baiclalein, lipooxygenase inhibitors, or by 10 μM ryanodine and thapsigargin, Ca2+store inhibitors. Conclusions: These results suggest that the relaxant effect of propofol may result from activation of BKCa channels by inhibiting voltage-gated Ca2+ influx in a prolonged manner.
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Hyun Il Seo,권성춘,Jae Young Kwak 대한외과학회 2022 Annals of Surgical Treatment and Research(ASRT) Vol.103 No.3
Purpose: We aimed to investigate the protective effect of sigma 1 receptor agonist and antagonist, PRE084 and BD1047, respectively, on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Methods: Thirty male ICR mice were randomly divided into 5 groups: control, 50% ethanol, colitis, PRE084 + colitis, and combined (PRE084 + BD1047 + colitis). Colitis was induced by intrarectal administration of TNBS. PRE084 and BD1047 were injected daily, starting 3 days before colitis induction. Distal colon tissue was excised for histopathological evaluation, and levels of glutathione (GSH), superoxide dismutase (SOD), myeloperoxidase (MPO), and lipid peroxidation were determined. Results: Colitis caused weight loss, mucosal damage, upregulation of tumor necrosis factor-α, interleukin (IL)-1β, IL- 6, MPO, and thiobarbituric acid reactive substance activities, and downregulation of GSH and SOD activities. These changes caused by TNBS-induced colitis were significantly ameliorated by PRE084 pretreatment. However, the combined pretreatment with BD1047 significantly attenuated the protective effect of PRE084, thereby reverting to the colitis-induced state. Conclusion: We conclude that the sigma 1 receptor agonist PRE084 exhibits significant protective effects against TNBS- induced colitis, which appears to be at least partly mediated by the inhibition of inflammation and oxidative stress, and enhancement of antioxidant properties. Collectively, these results suggest that PRE084 might be an effective drug for the treatment of ulcerative colitis.
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Forskolin Changes the Relationship between Cytosolic Ca2+ and Contraction in Guinea Pig Ileum
한군희,전갑진,연동수,권성춘 대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.3
This study was designed to clarify the mechanism of the inhibitory effect of forskolin on contraction, cytosolic Ca2+ level ([Ca2+]i), and Ca2+ sensitivity in guinea pig ileum. Forskolin (0.1 nM∼10μM) inhibited high K+ (25 mM and 40 mM)- or histamine (3μM)-evoked contractions in a concentration- dependent manner. Histamine-evoked contractions were more sensitive to forskolin than high K+- evoked contractions. Spontaneous changes in [Ca2+]i and contractions were inhibited by forskolin (1μM) without changing the resting [Ca2+]i. Forskoln (10μM) inhibited muscle tension more strongly than [Ca2+]i stimulated by high K+, and thus shifted the [Ca2+]i-tension relationship to the lower-right. In histamine-stimulated contractions, forskolin (1μM) inhibited both [Ca2+]i and muscle tension without changing the [Ca2+]i-tension relationship. In α-toxin-permeabilized tissues, forskolin (10μM) inhibited the 0.3μM Ca2+-evoked contractions in the presence of 0.1 mM GTP, but showed no effect on the Ca2+-tension relationship. We conclude that forskolin inhibits smooth muscle contractions by the following two mechanisms: a decrease in Ca2+ sensitivity of contractile elements in high K+- stimulated muscle and a decrease in [Ca2+]i in histamine-stimulated muscle.
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