• Proceedings of the PSK Conference
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• 2003.04a
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• pp.305.2-306
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• 2003

We aimed at determining bioavailability of chlorphenesin carbamate, a muscle relaxant, and developing a simple analysis in human blood using HPLC. A rapid and sensitive HPLC method was developed and validated using reverse-phase C 18 column with retention time and limit of quantification of toferisone being 8.6 min and 0.5 ng/$m\ell$, respectively. Quantification was performed at 260 nm with tolferison as internal standard. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.304.1-304.1
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• 2003

We aimed at determining bioavailability of tolperisone, a muscle relaxant. and developing a simple analysis in human blood using HPLC. A rapid and snsitive HPLC method was developed and validated using reverse-phase C18 column with retention time and limit of quantification of toferisone being 7.3 min and 20 ng/$m\ell$, respectively. Quantification was performed at 260 nm with chlorphenesin as internal standard. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.240.2-240.2
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• 2003

We aimed at determining bioavailability of procainarnide HCl, an antiarrhythmic drug, and developing a simple analysis in human blood using HPLC. A rapid and sensitive HPLC method was developed and validated using reverse-phase C18 column with retension time and limit of quantification of procainamide HCl being 2.58 min and 50ng/ml, respectively. Quantification was performed at 275 nm with caffeine as internal standard. The method involved a simple extraction. In order to study blood level profile in time, eight volunteers were enrolled and orally took 250 mg procainamide HCl once. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.5
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• pp.183-188
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• 2007

Using BHK cells with stable expression of cardiac $Na^+/Ca^{2+}$ exchanger(BHK-NCX1), reverse mode(i.e. $Ca^{2+}$ influx mode) of NCX1 current was recorded by whole-cell patch clamp. Repeated stimulation of reverse NCX1 produced a cytosolic $Ca^{2+}$-dependent long-term inactivation of the exchanger activity. The degrees of inactivation correlated with NCX1 densities of the cells and were attenuated by reduced $Ca^{2+}$ influx via the reverse exchanger. The inactivation of NCX1 was attenuated by(i) inhibition of $Ca^{2+}$ influx with reduced extracellular $Ca^{2+}$, (ii) treatment with NCX1 blocker($Na^{2+}$), and (iii) increase of cytoplasmic $Ca^{2+}$ buffer(EGTA). In BHK-NCX1 cells transiently expressing TRPV1 channels, $Ca^{2+}$ influx elicited by capsaicin produced a marked inactivation of NCX1. We suggest that cytoplasmic $Ca^{2+}$ has a dual effect on NCX1 activities, and that allosteric $Ca^{2+}$ activation of NCX1 can be opposed by the $Ca^{2+}$-dependent long-term inactivation in intact cells.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.244.1-244.1
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• 2003

We aimed at determining bioavailability of clonazepam, an anxiolytic drug, and developing a simple analysis in human blood using HPLC. A rapid and sensitive HPLC method was developed and validated using reverse-phase C18 column with retension time and limit of quantification of clonazepam being 2.58 min and 5hg/ml, respectively. Quantification was performed at 235 nm with p-hydroxybenzoic acid ethyl ester as internal standard. The method involved a simple extraction. In order to study blood level profile in time, sight volunteers were enrolled and orally took 6 mg clonazepam once. (omitted)

• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.211-219
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• 1996

The inhibitory effect of cyclosporin A (CsA) on nitric oxide production is not related to the immunosuppressive action of the drug, but to the renal toxicity and arterial hyper-tension. In this study the experimental interventions to reverse the inhibition of nitric oxide production by cyclosporin A in rat aortic smooth muscle cells were examined. CsA inhibited the accumulation of nitrite, the stable end product of nitric oxide, in culture media in a concentration $(0.1{\sim}100{\mu}g/ml)-dependent$ manner. The inhibitory effect of CsA on nitrite accumulation were not antagonized by arginine (10 mM), a substrate of nitric oxide synthase, nor by calcium ionophore A23187 $(7{\mu}M)$. Forskolin, an activator of adenylate cyclase, which enhanced iNOS induction at transcriptional level, completely reversed the inhibitory action of CsA on nitrite accumulation. However, PMA (2 nM) and PDB (50 nM), PKC activators, increased the inhibitory action of CsA on nitrite accumulalion. From these results, it is suggested that cyclic AMP-elevating agents may be candidates of therapeutic agents in prevention and treatment of renal toxicity and arterial hypertension induced by CsA. Among conventional antihypertensive drugs, calcium channel blockers and ${\alpha}-blockers$ are preferred to ${\beta}-blockers$.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.2
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• pp.177-183
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• 2016

We fortuitously observed a human neutrophil intracellular free-calcium concentration ($[Ca^{2+}]_i$) increasing activity in the commercially available phosphodiesterase I (PDE I), which is actually dried crude venom of Crotalus atrox. As this activity was not observed with another commercially available pure PDE I, we tried to find out the causative molecule(s) present in 'crude' PDE, and identified Lys49-phospholipase A2 (Lys49-PLA2 or K49-PLA2), a catalytically inactive protein which belongs to the phospholipase A2 family, by activity-driven three HPLC (reverse phase, size exclusion, reverse phase) steps followed by SDS-PAGE and LC-MS/MS. K49-PLA2 induced $Ca^{2+}$ influx in human neutrophils without any cytotoxic effect. Two calcium channel inhibitors, 2-aminoetoxydiphenyl borate (2-APB) ($30{\mu}M$) and SKF-96365 ($20{\mu}M$) significantly inhibited K49-PLA2-induced $[Ca^{2+}]_i$ increase. These results suggest that K49-PLA2 modulates $[Ca^{2+}]_i$ in human neutrophils via 2-APB- and SKF-96365-sensitive calcium channels without causing membrane disruption.

• Biomolecules & Therapeutics
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• v.19 no.3
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• pp.320-323
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• 2011

We conducted this study to investigate whether berberine signifi cantly affects MUC5AC mucin gene expression and mucin production induced by epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) from human airway epithelial cells. Confl uent NCI-H292 cells were pretreated with varying concentrations of berberine for 30 min and then stimulated with EGF, PMA or TNF-${\alpha}$ for 24 h. MUC5AC mucin gene expression and mucin production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Berberine was found to inhibit the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-${\alpha}$. Berberine also inhibited the production of MUC5AC mucin protein stimulated by the same inducers. This result suggests that berberine can regulate the expression of mucin gene and production of mucin protein, by directly acting on human airway epithelial cells.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.65-67
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• 2004

Dehydroevodiamine (DHED) is one of the bioactive components of the Chinese herbal medicine Wu-chu-yu-tang that has been shown to produce various pharmacological effects. In the present study, we investigated the pharmacokinetics of DHED after intravenous administration of two doses (2.5 and 5 mg/kg) in anesthetized rats. The plasma concentration of DHED was measured by reverse-phase high-performance liquid chromatography with UV detection. The mean area under the curve of the time-concentration profile was $21.9\;and\;53.9\;{\mu}g{\cdot}min/ml$ after the 2.5- and 5-mg/kg doses, respectively, and the volume of distribution was 1584.9 and 1580.6 ml following 2.5- and 5-mg/kg doses, respectively. Plasma concentration profiles versus time were compatible with a two-compartment model and first-order kinetics. The terminal elimination half-life was $91.8{\pm}16.6\;min$ and $78.7{\pm}11.9\;min$ in the dose of 2.5 and 5 mg/kg, respectively. This is the first report to study the pharmacokinetics of DHED in animals.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.4
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• pp.319-328
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• 2020

High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague-Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.