• The Korean Journal of Pain
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• v.37 no.1
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• pp.26-33
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• 2024

Background: Sitagliptin is an antidiabetic drug that inhibits dipeptidyl peptidase-4 enzyme. This study aimed to investigate the antinociceptive and anti-inflammatory effects of sitagliptin in formalin and carrageenan tests and determine the possible mechanism(s) of its antinociceptive activity. Methods: Male Swiss mice (25-30 g) and male Wistar rats (180-220 g) were used for formalin and carrageenan tests, respectively. In the formalin test, paw licking time and in the carrageenan test, paw thickness were considered as indexes of pain behavior and inflammation respectively. Three doses of sitagliptin (2.5, 5, and 10 mg/kg) were used in these tests. Also, several antagonists and enzyme inhibitors were used to evaluate the role of adrenergic, serotonergic, dopaminergic, and opioid receptors as well as the NO/cGMP/K_ATP pathway in the antinociceptive effect of sitagliptin (5 mg/kg). Results: Sitagliptin showed significant antinociceptive and anti-inflammatory effects in the formalin and carrageenan tests respectively. In the carrageenan test, all three doses of sitagliptin significantly (P < 0.001) reduced paw thickness. Pretreatment with yohimbine, prazosin, propranolol, naloxone, and cyproheptadine could not reverse the antinociceptive effect of sitagliptin (5 mg/Kg), which indicates that adrenergic, opioid, and serotonin receptors (5HT₂) are not involved in the antinociceptive effects. L-NAME, methylene blue, glibenclamide, ondansetron, and sulpiride were able to reverse this effect. Conclusions: NO/cGMP/K_ATP, 5HT₃ and D₂ pathways play an important role in the antinociceptive effect of sitagliptin. Additionally significant anti-inflammatory effects observed in the carrageenan test might contribute in reduction of pain response in the second phase of the formalin test.

• Analytical Science and Technology
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• v.29 no.4
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• pp.179-185
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• 2016

An effective analytical method has been developed for the determination of β-blockers(atenolol, metoprolol and propranolol) and 6 β-lactams(amoxicillin, penicillin G, cefaclor, cefadroxil, cephalexin and cephradine) in water samples using two different cartridges. The samples were extracted by solid-phase extraction (SPE) with the usage of polymeric hydrophile-lipophile balance(HLB cartridges) and strong cation-exchange mixed-mode polymeric sorbent (MCX cartridges). A XDB-C₁₈ column(1.8 μm; 3.0 mm × 100 mm) was used for the sufficient chromatographic resolution. The calibration curves showed good linearity with high correlation coefficients (>0.995). The method detection limits (MDL) and the limits of quantification(LOQ) were from 1.1 to 3.9 ng/L and from 5 to 13 ng/L, respectively. The method was applied for the determination of the target compounds in tributaries and raw water of the Han River and these were found at N.D. to 0.209 μg/L.

• The Korean Journal of Physiology
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• v.17 no.1
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• pp.45-54
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• 1983

Contractile responses of myocardium and vascular smooth muscle to angiotensin II were studied in isolated rabbit papillary muscles and aortic helical strips, with respect to the sensitivity and the mechanism of action. All experiments were performed in $HCO-_3\;-buffered Tyrode solution which was aerated with $3%\;CO_2-97%\;O_2$ and kept pH 7.35 at $35^{\circ}C$. Action potentials were measured by conventional microelectrode technique in the papillary muscles. Helical strips of vascular smooth muscle were prepared from the descending thoracic aorta of the rabbit. Angiotensin II elicited a positive inotropic effect in doses from $10^{-8}$ to $10^{-6}\;M$, and this effect was dose-dependent and characterized by a symmetrical increase of maximum dP/dt during contraction and relaxation phase. Slow responses (or slow action potentials) were induced by A. II $(10^{-6}\;M)$ in the papillary muscle hypopolarized by 27 mM $K^+$. These A. II-induced slow action potentials were eliminated by verapamil (2 mg/l), but not affected by propranolol $(10^{-5}\;M)$. In aortic helical strips, contractile force was increased dose-dependently in the range of $10^{-10}{\sim}10^{-7}\;M$ A. II. $ED_{50}$ in aorta was $3{\times}10^{-9}\;M$ A. II, whereas that in paillary muscle was $2.5{\times}10^{-7}\;M$ A. II. A. II contracted vascular smooth muscle in depolarizing concentration of $K^+$ (100 mM $K^+$), and also produced a sustained contraction even in the presence of verapamil and regitine. The results of this experiment suggest that the primarily important physiological role of A. II is the action on the blood vessel, and the positive inotropic effect of A. II in papillary muscle results from the increase of slow inward $Ca^{++}$ current, and that A. II-induced contraction of aorta is independent of transmembrane potential and associated with promoting bet transmembrane $Ca^{++}\;-influx$ and the mobilization of cellular $Ca^{++}$.