• Restorative Dentistry and Endodontics
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• v.24 no.1
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• pp.180-186
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• 1999

Eugenol has been reported to reduce odontogenic pain and is known to have a structure similar to capsaicin, a potent stimulant of certain nociceptors. We have hypothesized that the analgesic effect of eugenol may be due, in part, to inhibition of capsaicin-sensitive nociceptors. To test this hypothesis, we evaluate whether eugenol inhibits capsaicin-sensitive release of immunoreactive calcitonin generated peptide(iCGRP) from bovine dental pulp. Freshly extracted bovine incisors were transported to the lab. on ice, Spilitted and pulp tissue was removed. The tissue was chopped into 200${\mu}m$ slices. Dental pulp was superfused(340 ${\mu}l/min$) in vitro with oxygenated Kreb's buffer. Eugenol and vehicle(0.02% 2-hydroxyl-${\beta}$-cyclodextrin) were administered prior to stimulation of pulp with capsaicin and iCGRP was measured by RIA. The results were as follows: 1. Administration of eugenol has no effect on basal release of iCGRP. 2. In the vehicle treated group, capsaicin evoked a 2.5-fold increase over basal iCGRP levels. 3. Administration of eugenol(600 ${\mu}M$) reduced capsaicin evoked release of iCGRP by more than 40%(153.4${\pm}$41.1% vs 258.9${\pm}$21.7%). 4. 2-hydroxylpropyl-${\beta}$-cyclodextrin of less than 0.02% is found to be an effective vehicle to dissolve eugenol without evoking iCGRP release from dental bovine pulp. These data indicate that eugenol inhibits pulpal capsaicin-sensitive fibers and suggest that intracanal medicament of eugenol may relieve pain, in part, by this mechanism.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.241-247
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• 2014

To investigate the underlying mechanisms of C18 fatty acids (stearic acid, oleic acid, linoleic acid and ${\alpha}$-linolenic acid) on mast cells, we measured the effect of C18 fatty acids on intracellular $Ca^{2+}$ mobilization and histamine release in RBL-2H3 mast cells. Stearic acid rapidly increased initial peak of intracellular $Ca^{2+}$ mobilization, whereas linoleic acid and ${\alpha}$-linolenic acid gradually increased this mobilization. In the absence of extracellular $Ca^{2+}$, stearic acid ($100{\mu}M$) did not cause any increase of intracellular $Ca^{2+}$ mobilization. Both linoleic acid and ${\alpha}$-linolenic acid increased intracellular $Ca^{2+}$ mobilization, but the increase was smaller than that in the presence of extracellular $Ca^{2+}$. These results suggest that C18 fatty acid-induced intracellular $Ca^{2+}$ mobilization is mainly dependent on extracellular $Ca^{2+}$ influx. Verapamil dose-dependently inhibited stearic acid-induced intracellular $Ca^{2+}$ mobilization, but did not affect both linoleic acid- and ${\alpha}$-linolenic acid-induced intracellular $Ca^{2+}$ mobilization. These data suggest that the underlying mechanism of stearic acid, linoleic acid and ${\alpha}$-linolenic acid on intracellular $Ca^{2+}$ mobilization may differ. Linoleic acid and ${\alpha}$-linolenic acid significantly increased histamine release. Linoleic acid (C18:2: ${\omega}$-6)-induced intracellular $Ca^{2+}$ mobilization and histamine release were more prominent than ${\alpha}$-linolenic acid (C18:3: ${\omega}$-3). These data support the view that the intake of more ${\alpha}$-linolenic acid than linoleic acid is useful in preventing inflammation.

• The Korean Journal of Physiology
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• v.22 no.2
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• pp.319-332
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• 1988

The regulations of renal function and renin release are influenced by neural, humoral and physical factors. During the last decade, considerable progress has been made in the identification and characterization of these extrinsic renal control systems. Mechanisms intrinsic to the kidney are also important for renal function. These include the autoregulation of blood flow, and the local control of renin secretion. Fundamental questions regarding the mechanism of these intrinsic controls remain unanswered. Recently, endogenous renal adenosine has been claimed to influence the tubuloglomerular feedback control and renin release. Two subclasses of adenosine receptors $A_1{\;}and{\;}A_2$ have been described. The present experiment was carried out to evaluate the effects of $N_6-cyclohexyladenosine$ $(CHA,{\;}A_1{\;}selective)$ and 5'-N-ethylcarbox-amide adenosine $(NECA,{\;}A_2{\;}selective)$ on the renal function and renin release in the unanesthetized rabbit. Intra-renal arterial infusion of NECA $(0.3{\sim}10.0n{\;}mole/min/rabbit)$ or CHA $(0.03{\sim}10.0n{\;}mole/min/rabbit)$ caused a prompt and dose-dependent decrease in urine volume, glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction (FF), electrolyte excretion and free water clearance $(CH_2O)$, the effect being much more profound with CHA than with NECA. The NECA infusion resulted in a profound decrease of systemic blood pressure, but the CHA infusion did not. Both NECA and GHA infusions caused a prompt and dose-dependent decrease in renin secretion rate, again the effect being greater with CHA than with NEGA. These results suggest that both $A_1{\;}and{\;}A_2$ adenosine receptors may be involved in the intrinsic control of renal function and renin release, and that the $A_1$ receptors plays a more important role than the $A_2$ receptor in the regulation of renal fnction.

• Bulletin of the Korean Chemical Society
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• v.35 no.8
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• pp.2391-2399
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• 2014

Novel dual responsive pectin hydrogels composed from poly(acrylamidoglycolic acid-co-vinylcaprolactam)/Pectin (PAV-PC) and also PAV-PC hydrogels are used as templates for the production of silver nanoparticles. 5-Fluorouracil is an anticancer drug and has been loaded in situ into PAV-PC hydrogels. Structure and morphology characterization of PAV-PC hydrogels were investigated by fourier transform infrared spectroscopy, differential scanning calorimetry, thermo gravimetric analysis, X-ray diffraction studies, scanning electron microscopy and transmission electron microscopy. The results revealed a molecular level dispersion of the drug in PAV-PC hydrogels. In vitro release of 5-fluorouracil from the PAV-PC hydrogels has been carried out in GIT fluids as well as in various temperatures. 5-Fluorouracil released from PAV-PC hydrogels was 50% at pH 1.2, and 85% at pH 7.4 within 24 h. The release profile was characterized with PAV-PC hydrogels and initial burst effect was significantly reduced in two buffer media (1.2 and 7.4), followed by a continuous and controlled release phase, the drug release mechanism from polymer was due to Fickian diffusion. In situ fabrication of silver nanoparticles inside the hydrogel network via the reduction of sodium borohydrate by PAV-PC chains led to hydrogel nanocomposites. The diameter of the nanocomposites was about 50-100 nm, suitable for uptake within the gastrointestinal tract due to their nanosize range and mucoadhesive properties. These nanocomposite PAV-PC hydrogels showed strong antimicrobial activity towards Bacillus subtilis (G+ve) and Escherichia coli (G-ve).

• Archives of Pharmacal Research
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• v.26 no.9
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• pp.747-755
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• 2003

The aim of the present study was to clarify whether cotinine affects the release of catecholamines (CA) from the isolated perfused rat adrenal gland, and to establish the mechanism of its action, in comparison with the response of nicotine. Cotinine (0.3∼3 mM), when perfused into an adrenal vein for 60 min, inhibited CA secretory responses evoked by ACh (5.32 mM), DMPP (a selective neuronal nicotinic agonist, 100 $\mu$M for 2 min) and McN-A-343 (a selective muscarinic $M_1 -agonist, 100 \mu$ M for 2 min) in dose- and time-dependent manners. However, cotinine did not affect CA secretion by high $K^+$ (56 mM). Cotinine itself also failed to affect basal CA output. Furthermore, in the presence of cotinine (1 mM), CA secretory responses evoked by Bay-K-8644 (an activator of L-type $Ca^{2+}$ channels, 10 $\mu$ M) and cyclopiazonic acid (an inhibitor of cytoplasmic $Ca^{2+}-ATPase, 10 \mu$ M) were relative time-dependently attenuated. However, nicotine (30$\mu$ M), given into the adrenal gland for 60 min, initially rather enhanced CA secretory responses evoked by ACh and high $K^+$, followed by the inhibition later, while it time-dependently depressed the CA release evoked by McN-A-343 and DMPP. Taken together, these results suggest that cotinine inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors, but does fail to affect that by the direct membrane-depolarization. It seems that this inhibitory effect of cotinine may be exerted by the cholinergic blockade, which is associated with blocking both the calcium influx into the rat adrenal medullary chromaffin cells and $Ca^{2+}$ release from the cytoplasmic calcium store. It also seems that there is a big difference in the mode of action between cotinine and nicotine in the rat adrenomedullary CA secretion.

• Applied Chemistry for Engineering
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• v.30 no.2
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• pp.233-240
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• 2019

Molecular recognition technology has attracted considerable attention for improving the selectivity of a specific molecule by imprinting it on a polymer matrix. In this study, adsorption and release characteristics of chitosan based drug delivery films imprinted with sulindac (SLD) were investigated in terms of the plasticizer, temperature and pH and the results were also interpreted by the related mathematical models. The adsorption characteristics of target molecules on SLD-imprinted polymer films were better explained by the Freundlich and Sips equation than that of the Langmuir equation. The binding site energy distribution function was also useful for understanding the adsorption relationship between target molecules and polymer films. The drug release of SLD-imprinted polymer films followed the Fickian diffusion mechanism, whereas the drug release using artificial skin followed the non-Fickian diffusion behavior.

• Restorative Dentistry and Endodontics
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• v.47 no.4
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• pp.42.1-42.11
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• 2022

Objective: This study investigated the effects of various concentrations of sodium hypochlorite (NaOCl) on human whole-blood clotting kinetics, the structure of the blood clots formed, and transforming growth factor (TGF)-β1 release. Materials and Methods: Human whole blood was collected from 5 healthy volunteers and divided into 4 groups: CG (control, 0.5 mL of blood), BN_0.5 (0.5 mL of blood with 0.5 mL of 0.5% NaOCl), BN₃ (0.5 mL of blood with 0.5 mL of 3% NaOCl), and BN_5.25 (0.5 mL of blood with 0.5 mL of 5.25% NaOCl). The effects of NaOCl on clotting kinetics, structure of fibrin and cells, and release of TGF-β1 were assessed using thromboelastography (TEG), scanning electron microscopy (SEM), and enzyme-linked immunosobent assay, respectively. Statistical analysis was conducted using the Kruskal Wallis and Mann-Whitney U tests, followed by the post hoc Dunn test. A p value < 0.05 indicated statistical significance. Results: The blood samples in BN_0.5 and BN₃ did not clot, whereas the TEG of BN_5.25 showed altered clot formation. Samples from the CG and BN₃ groups could only be processed with SEM, which showed that the latter lacked fibrin formation and branching of fibers, as well as clumping of red blood cells with surface roughening and distortion. TGF-β1 release was significantly highest in BN₃ when all groups were compared to CG (p < 0.05). Conclusions: Each concentration of NaOCl affected the release of TGF-β1 from blood clots and altered the clotting mechanism of blood by affecting clotting kinetics and cell structure.

• Journal of Periodontal and Implant Science
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• v.35 no.2
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• pp.427-436
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• 2005

Objective: MMP-8 is a neutrophil enzyme and its level increases in some inflammatory diseases, including periodontal disease. We knew that the lipopolysaccharide of E.coli(E-LPS) induced MMP-8 release from human neutrophils. E-LPS is known to induce the production and release of inflammatory cytokines through CD14, Toll-like receptor(TLR). In the present study, we investigated whether MMP-8 release by E-LPS is induced via CD14-TLR pathway and the cellular mechanism of MMP-8 release in human neutrophils. Material and methods: Human neutrophils were isolated from the peripheral blood of healthy donors and pre-incubated in medium containing antibodies against CD14, anti-TLR2 and anti-TLR4 or several inhibitors of microtubules and microfilaments and then incubated with E-LPS. The cells were treated TPCK and E-LPS simultaneously. The MMP-8amount in the culture medium was determined using ELISA. Results: E-LPS increased MMP-8release from neutrophils and its induction was inhibited by anti-CD14 and anti-TLR4 but not by anti-TLR2 antibodies. The inhibitors of microtubule and microfilament polymerization significantly decreased E-LPS-induced MMP-8release. TPCK inhibited E-LPS-induced MMP-8 release. Conclusion: These results suggest that MMP-8 release is induced by E-LPS via the CD14-TLR4 signal pathway in human neutrophils and may be depedent on microtubule and microfilament systems and $NF-{\kappa}B$ pathway.

• The Journal of Korean Medicine
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• v.27 no.4
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• pp.74-83
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• 2006

Ssanghwatang (SHT) has been known to prove effective in the treatment for erectile dysfunction (ED), and its modified formula is widely used in clinical practice. However, its fundamental mechanism of action is not clearly known. It is well known that endothelial cells can achieve the relaxation of vascular smooth muscles by the release of nitric oxide (NO). NO is synthesized by the enzyme NO synthase (NOS) from L-arginine and oxygen. It is widely accepted that NO plays an important role in the relaxation of corpus cavernous smooth muscle and vasculature. In addition, in terms of the penile erection, the NO/cGMP pathway is more potent than the PCE1/cAMP pathway. The main purpose of the present study was to investigate the mechanism of the erectile effects of SHT by focusing on its direct effects on corpus cavernous smooth muscle cells. We investigated the NOS activity, nitrite concentration and cGMP levels in rat corpus cavernous smooth muscle cell lines activated by SHT extracts. Furthermore, we evaluated the effect of SHT extracts on penile smooth muscle relaxation following oral administration of SHT extract powder to rats by the dosage of 1 g/kg over fifteen days. As a result, we found that SHT stimulated NO release. NOS activity and cGMP levels were increased by SHT respectively. Furthermore, SHT relaxed the corpus cavernous smooth muscle. These results are consistent with the concept that penile erection by SHT is carried out through the NO/cGMP pathway. In conclusion, the present study shows that SHT increases the NOS activity, synthesizes NO and augments the cGMP, which mediates penile erection. Further determination of the SHT mechanism related with the NO/cGMP pathway strongly indicates that SHT can be used as a remedy for erectile impotence.

• Transactions of the Korean Society of Mechanical Engineers A
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• v.40 no.3
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• pp.275-280
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• 2016

In this study, a release test bed is designed to evaluate the dynamic behaviors of a coil spring. From the release tests, the dynamic behaviors of a coil spring are analyzed. A lumped parameter spring model was established for numerical simulation of a spring. The design variables of a coil spring are optimized by using the design of experiments approach. Two-level factorial designs are used for the design optimization, and the primary effects of the design variables are analyzed. Based on the results of the interaction analysis and design sensitivity analysis, the level of the design variables is rearranged. Finally, the mixed-level factorial design is used for the optimum design process. According to the optimum design of the opening spring, the dynamic performance of the spring-operated mechanism increases by 2.90.