• Korean Journal of Acupuncture
• /
• v.22 no.1
• /
• pp.117-132
• /
• 2005

Objectives : This study was carried out to determine whether Juglandis Semen herbal acupuncture (JSA) exerts the protective effect against toxic agent-induced live. cell damage. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring maiondialdehyde (MDA), a product of lipid peroxidation, in rabbit liver slices. Results : When tissues were incubated with 0.5 mM Hg for $10{\sim}120\;min$, LDH release and lipid peroxidation were increased as a function of incubation time, and these effects were significantly prevented by addition of 0.1% JSA. Hg increased LDH release and lipid peroxidation in dose-dependent manner over the range of $0.1{\sim}l\;mM$ concentrations, which were reduced by 0.1% JSA. When tissues were treated with 0.5 mM Hg in the presence of $0.05{\sim}l\;%$ JSA, LDH release and lipid peroxidation induced by Hg were prevented by JSA in a dose-dependent fashion. JSA at 0.5 and 1% prevented completely effects of 0.5 mM Hg. When tissues were treated with 0.5 mM Hg for 60 min, LDH release and lipid peroxidation were increased, which were significantly prevented by addition of 0.1 % JSA. tert-Butyl hydroperoxide (tBHP) increased LDH release and lipid peroxidation, which were significantly reduced by 0.1 % JSA. Such protective effects were similar to those of N,N'-diphenyl-p-phenylenediamine (DPPD), a potent antioxidant. When tissues were treated with 0.5 mM Hg, activities of catalase and glutathione peroxidase were inhibited, and glutathione content was also reduced. Such effects were prevented by JSA, but not by DPPD. JSA prevented Hg-induced morphological changes. Conclusions : These results indicate that JSA exerts the protective effect against liver cell injury induced by toxic agents through antioxidant action, and this effect may be attributed to an increase in activities of endogeous anitoxidant enzymes and GSH content. However, antioxidant effect of JSA is different from that of a well-known potent antioxidant DPPD.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.4
• /
• pp.393-404
• /
• 1999

We have reported that hypoxia stimulates EDRF(s) release from endothelial cells and the release may be augmented by previous hypoxia. As a mechanism, it was hypothesized that reoxygenation can stimulate EDRF(s) release from endothelial cells and we tested the hypothesis via bioassay experiment. In the bioassay experiment, rabbit aorta with endothelium was used as EDRF donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2a}\;(3{\times}10^{-6}\;M)$ which was added to the solution perfusing through the aorta. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $O_2/5%\;CO_2$ mixed gas. Hypoxia/reoxygenation were interexchanged at intervals of 2 minutes (intermittent hypoxia). In some experiments, endothelial cells were exposed to 10-minute hypoxia (continuous hypoxia) and then exposed to reoxygenation and intermittent hypoxia. In other experiments, the duration of reoxygenation was extended from 2 minutes to 5 minutes. When the donor aorta was exposed to intermittent hypoxia, hypoxia stimulated EDRF(s) release from endothelial cells and the hypoxia-induced EDRF(s) release was augmented by previous hypoxia/reoxygenation. When the donor aorta was exposed to continuous hypoxia, there was no increase of hypoxia-induced EDRF(s) release during hypoxia. But, after the donor aorta was exposed to reoxygenation, hypoxia-induced EDRF(s) release was markedly increased. When the donor aorta was pretreated with nitro-L-arginine $(10^{-5}$ M for 30 minutes), the initial hypoxia-induced EDRF(s) release was almost completely abolished, but the mechanism for EDRF(s) release by the reoxygenation and subsequent hypoxia still remained to be clarified. TEA also blocked incompletely hypoxia-induced and hypoxia/reoxygenation-induced EDRF(s) release. EDRF(s) release by repetitive hypoxia and reoxygenation was completely blocked by the combined treatment with nitro-L-arginine and TEA. Cytochrome P450 blocker, SKF-525A, inhibited the EDRF(s) release reversibly and endothelin antgonists, BQ 123 and BQ 788, had no effect on the release of endothelium-derived vasoactive factors. Superoxide dismutase (SOD) and catalase inhibited the EDRF(s) release from endothelial cells. From these data, it could be concluded that reoxygenation stimulates EDRF(s) release and hypoxia/reoxygenation can release not only NO but also another EDRF from endothelial cells by the production of oxygen free radicals.

• The Korean Journal of Physiology and Pharmacology
• /
• v.9 no.2
• /
• pp.87-94
• /
• 2005

It is not clear whether $Ca^{2+}-induced$ $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that $Ca^{2+}$ entry via voltage-gated L-type $Ca^{2+}$ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR $Ca^{2+}$ release in the regulation of ANP release and whether $Ca^{2+}$ entry via L-type $Ca^{2+}$ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR $Ca^{2+}$ release, increased atrial myocytic ANP release ($8.69{\pm}3.05$, $19.55{\pm}1.09$, $27.31{\pm}3.51$, and $18.91{\pm}4.76$% for 1, 2, 3, and $6{\mu}M$ ryanodine, respectively; all P<0.01) with concomitant decrease in atrial stroke volume and pulse pressure in a dose-dependent manner. In the presence of thapsigargin, an inhibitor of SR $Ca^{2+}$ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type $Ca^{2+}$ channel with nifedipine abolished ryanodine-induced increase in ANP release ($0.69{\pm}5.58$% vs. $27.31{\pm}3.51$%; P＜0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that $Ca^{2+}$-induced $Ca^{2+}$ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.

• Biomolecules & Therapeutics
• /
• v.6 no.4
• /
• pp.371-377
• /
• 1998

The aim of the present study was to investigate the effect of Palmiwon on the type 1-prediabetic models induced by streptozotocin (STZ) in RINm5F cells and HIT-T15 cells. Palmiwon increased the cell proliferation and insulin release when pre- and post-treated for the STZ-exposed pancreatic beta cells. The cell proliferation and insulin release of these beta cells were measured by $^3$H-thymidine uptake and RIA, respectively. We also analyzed nutrients such as sugars, fatty acid and amino acids and minerals containing in Palmiwon using by gas chromatography, amino acid analyzer and AA spectrometer, respectively. Palmiwon seems to have protective and recovery properties on the prediabetic model in cellular level, which were ascribe to various nutrients and minerals containing in Palmiwon. From these results, it could be suggested that Palmiwon may be available as preventive and therapeutic prescription of type 1 diabetes mellitus.

• Journal of the Korean Wood Science and Technology
• /
• v.8 no.2
• /
• pp.1-5
• /
• 1980

This study is carried out to determine the scavenging effect of resorcinol added into the urea formaldehyde resin on the formaldehyde release of plywood, as the preliminary study of using the phenolic substances. The method for formaldehyde determination used in this report is the improved chromotropic acid determination. The results are summarized as follows: 1. Resorcinol added into the urea formaldehyde adhesive acts as a good scavenger. 4 percent of resorcinol reduced the formaldehyde release to less than half content. 2. Adding resorcinol gave better glue shear strength than that of control, showing the peak of the shear strength, at 2 percent and decreased to the same strength as control along its content of 4 percent. 3. Moisture content of air dried plywood met the standard very well.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.27 no.2
• /
• pp.344-349
• /
• 1998

The purpose of this study was carried out to investigate the effect of scoparone(6, 7-dimethoxyco-umarin) on liver function. Sprague-Dawley rats were treated with scoparone at a dose of 20mg/kg body weight for 5 days. Hepatic bile flow, liver weight, BSP(bromosulfophthalein) biliary excretion, alanine aminotransferase(ALT) and aspartate aminotransferase(AST) activities, malondialdehyde production and lactate dehydrogenase(LDH) release were assayed. Among them, ALT and AST activities, malondialdehyde production and LDH release were assayed by using primary hepatocyte cultures at a concentration of 0.1mg/ml. Scoparone treatment had no effect on liver weight and hepatic bile flow. Scoparone treatment not only increased BSP biliary excretion, but also recovered the decreased BSP biliary excretion by CCl4, Also scoparone significantly decreased with the increases of ALT and AST activities, malondialdehyde production and LDH release induced by CCl4. These results suggested that scoparone could protect the liver damage by chemicals via promoting the liver excretory function.

• The Korean Journal of Physiology and Pharmacology
• /
• v.10 no.2
• /
• pp.101-108
• /
• 2006

The aim of the present study was to elucidate whether gallic acid could modulate the inflammatory allergic reaction and to study its mechanism of action Gallic acid inhibited compound 48/80- or immunoglobulin E (IgE)-induced histamine release from mast cells. The inhibitory effect of gallic acid on the histamine release was mediated by modulation of cAMP and intracellular calcium. Gallic acid decreased the phorbol 12-myristate 13-acetate plus calcium ionophore A23187-stimulated pro-inflammatory cytokine gene expression and production such as TNF- ${\alpha}$ and IL-6 in human mast cells, and the inhibitory effect of gallic acid was on dependent nuclear factor- ${\kappa}$B and p38 mitogen-activated protein kinase. Our findings provide evidence that gallic acid inhibits mast cell-derived inflammatory allergic reaction by blocking histamine release and pro-inflammatory cytokine expression.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.1
• /
• pp.31-39
• /
• 1998

As it has been reported that the depolarization induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1$ adenosine heteroreceptor and various lines of evidence suggest the $A_2$ adenosine receptor is present in the hippocampus. The present study was undertaken to delineate the role of adenosine receptors on the hippocampal ACh release. Slices from the rat hippocampus were equilibrated with $[^3H]choline$ and then the release amount of the labelled product, $[^3H]ACh$, which was evoked by electrical stimulation (rectangular pulses, 3 Hz, 2 ms, 24 mA, $5\;V/cm^{-1}$, 2 min), was measured, and the influence of various adenosine receptor-related agents on the evoked tritium outflow was investigated. And also, the drug-receptor binding assay was performed in order to confirm the presence of $A_1$ and $A_2$ adenosine receptors in the rat hippocampus. N-ethylcarboxamidoadenosine (NECA), a potent adenosine receptor agonist with nearly equal affinity at $A_1$ and $A_2$ adenosine receptors, in concentrations ranging from $1{\sim}30\;{\mu}M$, decreased the electrically-evoked $[^3H]ACh$ release in a concentration-dependent manner without affecting the basal rate of release. And the effect of NECA was significantly inhibited by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 2 ${\mu}M$), a selective $A_1$ adenosine receptor antagonist, but was not influenced by 3,7-dimethyl-1-propargylxanthine (DMPX, 5 ${\mu}M$), a specific $A_2$ adenosine receptor antagonist. $N^6-cyclopentyladenosine$ (CPA), a selective $A_1$ adenosine receptor agonist, in doses ranging from 0.1 to 10 ${\mu}M$, reduced evoked $[^3H]ACh$ release in a dose-dependent manner without the change of the basal release. And the effect of CPA was significantly inhibited by 2 ${\mu}M$ DPCPX treatment. 2-P-(2-carboxyethyl)-phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride (CGS-21680C), a potent $A_2$ adenosine receptor agonist, in concentrations ranging from 0.1 to 10 ${\mu}M$, did not alter the evoked ACh release. In the drug-receptor binding assay, the binding of $[^3H]2-chloro-N^6-cyclopentyladenosine$ ($[^3H]$CCPA) to the $A_1$ adenosine receptor of rat hippocampal membranes was inhibited by CPA ($K_i$ = 1.22 nM), NECA ($K_i=10.17 nM$) and DPCPX ($K_i=161.86 nM$), but not by CGS-21680C ($K_i=2,380 nM$) and DMPX ($K_i=22,367 nM$). However, the specific binding of $[^3H]CGS-21680C$ to the $A_2$ adenosine receptor was not observed. These results suggest that the $A_1$ adenosine heteroreceptor play an important role in evoked ACh release, but the presence of $A_2$ adenosine receptor is not confirmed in this study.

• The Korean Journal of Pharmacology
• /
• v.32 no.2
• /
• pp.127-138
• /
• 1996

The effects of adenosine analogues on the electrically-evoked acetylcholine(ACh) release and the influence of ischemia on the effects were studied in the rat hippocampus. Slices from the rat hippocampus were equilibrated with $0.1{\mu}M$ $[^3H]-choline$ and the release of the labelled product, $[^3H]-ACh$, was evoked by electrical stimulation(3 Hz, 2 ms, 5 $VCm^{-1}$ and rectangular pulses for 2 min), and the influence of various agents on the evoked tritiumoutflow was investigated. Ischemia(10 min with 95% $N_2$ + 5% $CO_2$) increased both the basal and evoked ACh release. These increases were abolished by glucose addition into the superfused medium, and they significantly inhibited either by 0.1 & $0.3{\mu}M$ TTX pretreatment or by removing $Ca^{++}$ in the medium. MK-801($1{\sim}10{\mu}M$), a specific NMDA receptor antagonist, and glibenclamide $(1{\mu}M)$, a $K^+-channel$ inhibitor, did not alter the evoked ACh release and nor did they affect the ischemia-induced increases In ACh release. However, polymyxin B(0.03 mg), a specific protein kinase C inhibitor, significantly inhibited the effects of ischemia on the evoked ACh release. Adenosine and $N^6-cyclopentyladenosine$ decreased the ACh release in a dose dependent manner in ischemic condition, though the magnitude of inhibition was far less than those in normal(normoxic) condition. However, the treatment with $5{\mu}M$ DPCPX, a potent $A_1-adenosine$ receptor antagonist, potentiated the ischemia-effect. These results indicate that the evoked-ACh release is potentiated by ischemia, and this process being most probably mediated by protein kinase C, and that the decreased effect of ACh release mediated by $A_1-adenosine$ receptor is significantly inhibited in ischemic state.

• Journal of Korean Medicine Rehabilitation
• /
• v.23 no.3
• /
• pp.201-210
• /
• 2013

The purpose of this study is to evaluate the effect of active release technique on sequelae of tibial plateau fracture. Two patients with sequelae of tibial plateau fracture were treated with active release technique. Visual analog scale (VAS), Lysholm knee scoring scale, range of motion were used to measure changes during treatment. After treatment, visual analog scale, Lysholm knee scoring scale, range of motion were improved significantly. Active release technique showed significant improvement to the sequlae of tibial plateau fracture that were showing no signs of improvement for twelve and eighteen weeks. This clinical trial showed that active release technique has meaningful effect on sequlae of tibial plateau fracture and more research should be followed.