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JYMS : Journal of Yeungnam Medical Science

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Hyoung Chul Choi 7 Articles
Effects of AMP-activated Protein Kinase Activating Compounds and Its Mechanism.
Hyoung Chul Choi
Yeungnam Univ J Med. 2012;29(2):77-82.   Published online December 31, 2012
DOI: https://doi.org/10.12701/yujm.2012.29.2.77
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AbstractAbstract PDF
AMP-activated protein kinase (AMPK) is an important cellular fuel sensor. Its activation requires phosphorylation at Thr-172, which resides in the activation loop of the alpha1 and alpha2 subunits. Several AMPK upstream kinases are capable of phosphorylating AMPK at Thr-172, including LKB1 and CaMKKbeta (Ca2+/calmodulin-dependent protein kinase kinasebeta). AMPK has been implicated in the regulation of physiological signals, such as in the inhibition of cholesterol fatty acid, and protein synthesis, and enhancement of glucose uptake and blood flow. AMPK activation also exhibits several salutary effects on the vascular function and improves vascular abnormalities. AMPK is modulated by numerous hormones and cytokines that regulate the energy balance in the whole body. These hormone and cytokines include leptin, adiponectin, ghrelin, and even thyroid hormones. Moreover, AMPK is activated by several drugs and xenobiotics. Some of these are in being clinically used to treat type 2 diabetes (e.g., metformin and thiazolidinediones), hypertension (e.g., nifedipine and losartan), and impaired blood flow (e.g., aspirin, statins, and cilostazol). I reviewed the precise mechanisms of the AMPK activation pathway and AMPK-modulating drugs.

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Effect of Progesterone on COX-2 Expression and Proliferation of Prostate Stromal Cell.
Soo Ryun Jung, Sung Han Kim, E Hwa Choi, Ji Eun Park, Eun Mi Jeon, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi
Yeungnam Univ J Med. 2006;23(1):62-70.   Published online June 30, 2006
DOI: https://doi.org/10.12701/yujm.2006.23.1.62
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AbstractAbstract PDF
BACKGROUND
Benign prostatic hyperplasia (BPH) is the most common benign tumor in older men; the etiology of this disease remains poorly understood. Testosterone and dihydrotestosterone (DHT) both act as androgen via a single androgen receptor. Testosterone is converted to DHT by 5alpha-reductase in prostatic stromal cells. Progesterone has been reported to inhibit DHT conversion; howevwe, its effect on prostatic stromal cells remains to be elucidated. MATERILAS AND METHODS: In this experiment, we investigated the effect of progesterone on androgen receptor expression induced by DHT. We also tested the effect of progesterone on cyclooxygenase-2 (COX-2) expression, as well as prostate stromal cell proliferation using the cell count kit-8. RESULTS: Progesterone did not cause an increase of prostate stromal cell proliferation. The mRNA expression of the androgen receptor and COX-2 were not changed by progesterone; the expressions of androgen receptor and COX-2 proteins were decreased by progesterone in prostate stromal cells. CONCLUSION: These results suggest that in prostate stromal cells, progesterone decreases androgen receptor protein expression, which results in decrement of COX-2 protein expression. This effect might be mediated by post-transcriptional regulation.
Effects of Cyclooxygenase Inhibitors on Vascular Reactivity and Alterations of Cyclooxygenase Expression.
Ki Young Lee, Jin Woo Park, Eun A Eum, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi
Yeungnam Univ J Med. 2006;23(1):36-44.   Published online June 30, 2006
DOI: https://doi.org/10.12701/yujm.2006.23.1.36
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AbstractAbstract PDF
BACKGROUND
There is controversy regarding whether COX-2 specific inhibitors are associated with elevation of blood pressure. We compared the effects of aspirin, indomethacin, and celecoxib for vascular reactivity induced by phenylephrine. We also tested the effects of indomethacin and NO donor on COX-1 and COX-2 protein expression, as well as nitrite production in culture medium of vascular smooth muscle cells. MATERILAS AND METHODS: In this experiment, we used the isometric tension study for vascular reactivity. After 45 minutes of pretreatment with aspirin, indomethacin, celecoxib, and phenylephrine induced contractions were tested. COX-1 and COX-2 protein expressions were analyzed by Western blot and nitrite production by the Griess reaction. RESULTS: Although celecoxib pretreatment caused enhanced arterial contraction, aspirin pretreatment induced more potent arterial contraction than celecoxib in the isometric tension study of rabbit femoral artery. COX-1 protein expression was unchanged by indomethacin, SNP and NOR-3; COX-2 protein expression was increased by the addition of indomethacin, SNP, and NOR-3. Especially, NOR-3, a NO donor, significantly increased COX-2 protein expression with unstimulated conditions as well as LPS stimulation. Induction of nitrite production was higher with NOR-3 treatment than SNP treatment with LPS stimulation. CONCLUSION: These results suggest that aspirin caused more potent vascular contraction than celecoxib and indomethacin. COX-2 expression in VSMC depended on the types of NO donor and LPS stimulation.
The Effects of Ethanol on Cholinesterase Inactivation by Organophosphorous.
Hyoung Chul Choi, Jong Ho Kim, Jeoung Hee Ha, Kwang Yoon Lee, Won Joon Kim, Hyun Jae Woo, Chang Uk Huh, Soo Min Son, Eun Jin Chun
Yeungnam Univ J Med. 1999;16(2):326-332.   Published online December 31, 1999
DOI: https://doi.org/10.12701/yujm.1999.16.2.326
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AbstractAbstract PDF
BACKGROUND
In korea the agricultural community widely uses organophosphorous, and organophosphorous poisonings are increasing every year. We compared change in activity of acetylcholinesterase and pseudocholinesterase by organophosphorous and by the interaction of ethanol and organophosphorous. We also compared the effect of reversible anticholinesterase drugs, physostigmine and neostigmine. The object of this study is to investigate the effects of several anticholinesterase drugs and on how ethanol influences the activity of cholinesterase. MATERIALS AND METHODS: Fifteen male university students were randomly selected, and blood samples were taken from the antecubital vein. The acetylcholinesterase in the RBC and the pseudocholinesterase in the serum were extracted and separated. The enzyme activity change was measured by the electrometric method. After adding acetylcholine, the pH change was measured with a pH meter. RESULTS AND CONCLUSION: Our results indicated that reversible anticholinesterase drugs decreased the cholinesterase activity more efficiently than organophosphorous. The acetyl cholinesterase and pseudocholinosterase activity were decreased by ethanol. When ethanol was added, oxime a cholinesterase activator, increased acetylcholinesterase activity but dose not increased pseudocholinesterase activity.
The Effects of Anticholinesterase Drugs on Gastric Motility.
Hyoung Chul Choi, Jong Ho Kim, Jeoung Hee Ha, Kwang Yoon Lee, Won Joon Kim, Dong Suk Kwak, Sung Hee Kim, Phil Hyun Song, Ji Hyun Yeo
Yeungnam Univ J Med. 1999;16(2):318-325.   Published online December 31, 1999
DOI: https://doi.org/10.12701/yujm.1999.16.2.318
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AbstractAbstract PDF
BACKGROUND
Anticholinesterase drug inhibits acetylcholinesterase(AChE), induce accumulation of acetylcholine(ACh) near cholinergic receptors and cholinergic stimulation. This experiment was performed to study the effects of anticholinesterase drugs on gastric motility and the effect of ethanal on anticholinesterase drug-induced motility change. MATERIALS AND METHODS: After excision of stomach, 2x10mm circular musele strips were made, which were then fixed to the isolated muscle chamber. An isometric tension transducer was used to measure the contraction change of the gastric smooth muscle strips after drug addition. RESULTS: Fenthion, and irreversible anticholinesterase drug, increased ACh induced contraction of gastric smooth muscle strips and PAM, a cholinesterase activator, antagnized this action. Physostigmine, a reversible anticholinesterase drug, also increased the ACh induced contraction. The gastric motility was decreased by PAM. Ethanol, which is known to induce smooth muscle relaxation, inhibited the increase of contraction by fenthion. CONCLUSION: These results indicate that irreversible and reversible anticholinesterase drugs increase gastric motility and antagonized by cholinesterase activating drugs. And when exposed to both ethanol and anticholinesterase drug, gastric motility was decreased by the smooth muscle relaxation effect by ethanal.
Effect of NG-nitro-L-arginine methyl ester and Methylene Blue on the Endotoxin-induced Vascular Hyporesponsiveness.
Hyoung Chul Choi, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim, Uy Dong Sohn
Yeungnam Univ J Med. 1997;14(2):337-349.   Published online December 31, 1997
DOI: https://doi.org/10.12701/yujm.1997.14.2.337
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  • 3 Download
AbstractAbstract PDF
The study was undertaken to examine the intensity of involvement of inducible nitric oxide synthase(iNOS) and cyclic GMP signal transduction pathway as one of the mechanisms of vaso-relaxative action of bacterial lipopolysaccharide (LPS) on the canine femoral artery strips. Canine femoral arteries were isolated and spiral strips of 10 mm long and 2 mm wide were made in the Tyroad solution of 0-4degrees C. The strips were prepared for isometric myography in Biancani's isolated muscle chamber contaning 1 ml of Tyrode solution, which was maintained with pH 7.4 by areation with 95% O2/5% CO2 at 37degrees C and nitric oxide (NO) production was measured simulltaneously with isolated nitric oxide mrter. LPS induced NO production, suppressed the phenylephrine (PE) induced contraction and enhanced the acetylcholine (ACh) induced relaxation. NG-nitro-L-arginine methyl ester (L-NAME), an NOS inhibitor, methylene blue, a guanylyl cyclase inhibitor, potentiated PE induced contraction and suppressed ACh induced relaxation on the LPS treated strips. The inhibitory potency of methylene blue for LPS induced vascular hyporeponsiveness was stronger than that of L-NAME. These result suggest that in canine femoral artery, both iNOS and cyclic GMP signal transduction pathway are related with LPS indused vascular hyporeponsiveness, but in minor with iNOS and in major with cyclic GMP signal transduction pathway.
Effect of Baclofen on the Cholinergic Nerve Stimulation in Isolated Rat Detrusor
Kwang Youn Lee, Keun Mi Lee, Eun Mee Choi, Hyoung Chul Choi, Jeoung Hee Ha, Won Joon Kim
Yeungnam Univ J Med. 1995;12(2):246-259.   Published online December 31, 1995
DOI: https://doi.org/10.12701/yujm.1995.12.2.246
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AbstractAbstract PDF
This study aimed to investigate the mechanism of action of baclofen on the detrusor muscle isolated from rat. Rats (Sprague-Dawley) were sacrificed by decapitation and exsanguination. Horizontal muscle strips of 2 mm × 15 mm were prepared for isometric myography in isolated muscle chamber bubbled with 95% / 5%-OZ / CO2 at 371C, and the pH was maintained at 7.4. Detrusor strips contracted responding to the electrical field stimulation (EFS) by 2 Hz, 20 msec, monophasic square wave of 60 VDC. The initial peak of EFS-Induced contraction was tended to be suppresed by α,β-methylene-adenosine 5'-triphosphate (mATP), a partial agonist of purinergic receptor, and baclofen, a GABAB receptor agonist (statistically nonsignificant). The late sustained contraction by EFS was suppressed significantly (p<0.05) by additions of atropine, a cholinergic muscarinic receptor antagonist and baclofen. The adenosine 5'-triphosphate-induced contraction was completely abolished by mA TP but not by baclofen. In the presence of atropine, the subsequent addition of acetylcholine could not contract the muscle strips: but the addition of acetylcholine in the presence of baclofen evoked a contraction to a remarkable extent. These results suggest that in the condition of present study, the cholinergic innervation may play a more important role than the purinergic one, and baclofen suppresses the contractility of rat detrusor by the stimulation of the GABA receptors to inhibit the release of neurotransmitter from the cholinergic nerve ending

JYMS : Journal of Yeungnam Medical Science