Effect of antioxidant in an acute lung injury animal model

강형섭,김기범,박혜민,고현규,김상진,김진상,김성종 한국화학공학회 2012 Korean Journal of Chemical Engineering Vol.29 No.11

The objective of this study was to scrutinize the involvement of nitric oxide (NO) and the diagnosis of blood in ARDS in a rat model determined by the sequential exposure to lipopolysaccharide (LPS). Also, the present study was designed to evaluate the effects of taurine and dexamethasone on ARDS induced by LPS. Measurements of nitrite/nitrate were elevated in BAL of LPS challenged rats, indicative of an induction of the NO synthase. Taurine and dexamethasone abrogated the extent of endotoxin-induced ARDS, as evidenced by the decreases BAL nitrate/nitrite,BALF protein and lung pathology. T+L+D-group had higher PaO2 and lower PaCO2 values than L-group and T+Lgroup. But, ionized Ca2+ and Mg2+ both were not shown significant change. Also, T+L and T+L+D-group showed significant increase compared with L-group, but for the other side no significant difference was seen between T+L and T+L+D group. We suggest that taurine and dexamethasone may be a drug of choice for preventing ARDS.

흰쥐 대동맥에서 cyclic nucleotide phosphodiesterase 억제제들의 혈관 이완 특성

강형섭,최철호,김진상,Kang, Hyung-sub,Choi, Cheol-ho,Kim, Jin-shang 대한수의학회 2003 大韓獸醫學會誌 Vol.43 No.4

Vascular smooth muscle relaxation is modulated by an increase in cGMP subsequent to nitric oxide (NO) production by endothelial cells. The effects of cAMP and cGMP phosphodiesterase (PDE) inhibitors were investigated in phenylephrine-precontracted rat aorta rings by using the specific inhibitors of PDE I, III, IV and V as relaxing agents (calmodulin-activated PDE inhibitors, IBMX and $W_7$, type I; cAMP-specific PDE inhibitors, milrinone, type IV; Ro 20-1724, type III and cGMP-specific PDE inhibitor, zaprinast, type V). All the PDE inhibitors produced a concentration-dependent relaxation in the ring with intact endothelium (+E). Except for milrinone, all the PDE inhibitors-induced relaxations were inhibited by removal of extracellular $Ca^{2+}$, $N^G$-nitro-L-arginine, $N^G$-nitro-L-arginine methyl ester, methylene blue (MS) or nifedipine. The specific PDE I and PDE IV inhibitors both produced endothelium-independent relaxations which were inhibited by MS in -E rings. However, zaprinast had no effect in -E rings. Except for milrinone, sodium nitroprusside (a NO donor)-induced relaxation was significantly augmented by all PDE inhibitors in +E rings. The results suggest that I) the vasorelaxant properties of IBMX, $W_7$, Ro 20-1724 and zaprinast are dependent on endothelium or on interaction with $Ca^{2+}$ regulation, 2) each PDE is differently distributed in vascular tissues (endothelial and smooth muscle cells), 3) the vasodilations of PDE inhibitors are due to the increase of cAMP and cGMP formation through inhibition of cAMP- and cGMP-PDE and 4) the vasodilation action of milrinone does not involve in endothelial-cyclic nucleotide system.

흰쥐 대동맥에서 imipramine의 혈관이완 작용기전

강형섭,이상우,백성수,조성건,김진상,Kang, Hyung-sub,Lee, Sang-woo,Baek, Sung-su,Joe, Sung-gun,Kim, Jin-shang 대한수의학회 2003 大韓獸醫學會誌 Vol.43 No.4

Although the antidepressant effects of imipramine (IMI) have been well known in several studies, the effects on cardiovascular system, particularly the vasorelaxant effects, have not known clearly. We hypothesis that IMI-induced vasorelaxation involves NO (nitrie oxide), activation of guanylate cyclase (GC) and $Ca^{2+}$ channel. The possible roles of the endothelium and $Ca^{2+}$ in IMI-induced responses were investigated using isolated rings of rat thoracic aorta and anesthesized rats. In KCl-precontracted rings. IMI produces endothelium-dependent and endothelium-independent relaxations in intact (+E) as well as endothelium-denuded (-E) rat aorta in a concentration-dependent manner. In phenylephrine (PE)-precontracted rings, the IMI-induced relaxation was significantly greater in +E rings. The IMI-induced relaxations were suppressed by nitric oxide synthase (NOS) inhibitors, N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, a non-selective GC inhibitor, methylene blue, $Na^+$ channel blockers, lidocaine and procaine, or $Ca^{2+}$ channel blockers, nifedipine and verapamil, in PE-precontracted +E rings, but not in PE-precontracted -E rings. These relaxations were also suppressed by lidocaine or procaine in -E aortic rings. However, IMI-induced relaxations were not inhibited by a PLC inhibitor 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC), an inositol monophosphatase inhibitor, lithium, indomethacin and dexamethasone in +E and -E rings. In vivo, infusion of IMI elicited significant decrease in arterial blood pressure. After intravenous injection of saponin, NOS inhibitors. MB and nifedipine, infusion of IMI inhibited the IMI-lowered blood pressure markedly. These findings suggest that the endothelium-dependent relaxation induced by IMI is mediated by activation of NO/cGMP signaling cascade or inhibition of $Ca^{2+}$ entry through voltage-gated channel, and this mechanism may contribute to the hypotensive effects of IMI in rats.

Mouse 갑상선에서 α₁-adrenoceptor 자극에 의한 thyroxine 유리 억제기전

강형섭,김송규,강창원,김진상,이호일,Kang, Hyung-sub,Kim, Song-kyu,Kang, Chang-won,Kim, Jin-sang,Lee, Ho-il 대한수의학회 1998 大韓獸醫學會誌 Vol.38 No.4

Thyroid function is mainly regulated through cAMP and phophatidylinositol, and it is well known that TSH-stimulated thyroxine ($T_4$) release is inhibited by catecholamine from mouse thyroids via the ${\alpha}_1$-adrenoceptor stimulation. Previous study has established that the inhibition of $T_4$ release by ${\alpha}_1$-adrenoceptor stimulation results in activated protein kinase C (PKC). The purpose of this study was to determine if ion transport systems are involved in the inhibition of $T_4$ release elicited by ${\alpha}_1$-adrenergic agonist in mouse thyroids. TSH-, IBMX- and cAMP analogue-stimulated $T_4$ release were significantly inhibited by methoxamine, R59022 (diacylglycerol kinase inhibitor), and MDL (adenylate cyclase inhibitor). TSH-stimulated $T_4$ release could be inhibited by Bay K 8644 and cyclopiazoic acid, but not by verapamil and tetrodotoxin. The addition of nifedipine ($Ca^{2+}$ channel blocker), tetrodotoxin and lidocaine ($Na^+$ channel blockers), but not amiloride (EIPA) and ryanodine, completely blocked the inhibitory effects of methoxamine on $T_4$ release. TSH-stimulated $T_4$ release was also inhibited by benzamil ($Na^+-Ca^{2+}$ exchange inhibitor). TSH-, IBMX- and cAMP-stimulated $T_4$ release were inhibited by methoxamine or R59022, these effects were reversed by nifedipine. but not by verapamil. Furthermore, nifedipine reversed the inhibitory effects of benzamil and R59022 on TSH-stimulated $T_4$ release. These data suggest that the observed ${\alpha}_1$-adrenoceptor-mediated inhibition of $T_4$ release in mouse thyroids is the result of an increase in intracellular $Na^+$ or $Ca^{2+}$ effected via activation of fast $Na^+$ or nifedipine-sensitive $Ca^{2+}$ channels, and that $Na^+-Ca^{2+}$ exchange may play an important role in reducing thyroid hormone by increasing intracellular $Ca^{2+}$.

흰쥐의 심장과 심근세포에서 dopaminergic 수용체 자극이 Mg²⁺ 조절에 미치는 영향

강형섭,김종식,김진상,Kang, Hyung-sub,Kim, Jong-shick,Kim, Jin-shang 대한수의학회 1999 大韓獸醫學會誌 Vol.39 No.3

Magnesium($Mg^{2+}$) is one of the most abundant intracellular divalent cation. Although recent studies demonstrate that adrenergic receptor stimulation evokes marked changes in $Mg^{2+}$ homeostasis, the regulation of $Mg^{2+}$ by dopaminergic receptor stimulation is not yet known. In this work, we used dopaminergic agents to identify which type(s) of receptors were involved in the mobilization of $Mg^{2+}$ by dopaminergic receptor stimulation in the perfused rat hearts, isolated myocytes and circulating blood. The $Mg^{2+}$ content was measured by atomic absorbance spectrophotometry. Dopamine(DA), apomorphine(APO) and pergolide stimulated $Mg^{2+}$ efflux in the perfused rat hearts and these effects were inhibited by haloperidol or fluphenazine, nonselective dopaminergic antagonists. SKF38393, a selective doparminergic agonist, increased $Mg^{2+}$ efflux from the perfused hearts in dose dependant manners and SKF38393-induced $Mg^{2+}$ efflux was blocked by haloperidol. However, dopaminergic agonists-induced $Mg^{2+}$ efflux was potentiated in the presence of sulpiride or eticlopride, $D_2$-selective antagonist, from the perfused hearts. This increase of $Mg^{2+}$ efflux was blocked by haloperidol or imipramine. DA or pergolide increased in circulating $Mg^{2+}$ from blood. By contrast, PPHT stimulated $Mg^{2+}$ influx(a decrease in efflux) from the perfused hearts and circulating blood. PPHT-induced $Mg^{2+}$ influx was blocked by fluphenazine in the perfused hearts. DA-stimulated $Mg^{2+}$ efflux was inhibited by dopaminergic antagoinst in the isolated myocytes. In conclusion, the flux of $Mg^{2+}$ is modulated by DA receptor activation in the rat hearts. The efflux of $Mg^{2+}$ can be increased by $D_1$-receptor stimulation and decreased by $D_2$-receptor stimulation, respectively.

흰쥐의 심장과 심근세포에서 cyclic AMP에 의한 Mg²⁺ 유리조절

강형섭,김진상,강창원,이호일,Kang, Hyung-sub,Kim, Jin-shang,Kang, Chang-won,Lee, Ho-il 대한수의학회 1999 大韓獸醫學會誌 Vol.39 No.1

Although it has been reported that hormones or chemicals, which increase in intracellular cAMP, produced $Mg^{2+}$ release from the heart, it is not well characterized whether a specific $Mg^{2+}$ exchanger is involved in cAMP-induced $Mg^{2+}$ efflux in the mammalian hearts. In this work, we studied the relationship between the increase in intracellular cAMP and ion transport system on $Mg^{2+}$ regulation in the perfused rat heart and isolated myocytes. The $Mg^{2+}$ content in the perfusate and supernatant were measured by atomic absorption spectrophotometer. The addition of membrane permeable cAMP analogue to the perfused hearts and myocytes induced a $Mg^{2+}$ efflux in the dose dependent manners. $Mg^{2+}$ efflux was stimulated by cAMP modulators (forskolin, IBMX and Ro20-1724) in the perfused hearts and myocytes. cAMP-induced $Mg^{2+}$ efflux was inhibited by $H_7$, benzamil or imipramine in the perfused hearts and myocytes, but not by EIPA. We confirmed that a significant $Mg^{2+}$ efflux was induced by an increase in intracellular cAMP in the hearts and myocytes. The cAMP-induced increase of $Mg^{2+}$ efflux in the hearts may be involved in ion transport system ($Na^+-Ca^{2+}$ and $Na^+-Mg^{2+}$ exchanger).

기니픽 심장과 심근 세포에서 ${\alpha}_1-Adrenergic$ 자극에 의한 $Mg^{2+}$ 유리조절

강형섭,장성은,김진상,Kang, Hyung-Sub,Chang, Sung-Eun,Kim, Jin-Sang 대한약리학회 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.6

$Mg^{2+}$ is the fourth most abundant cation in cellular organisms. Although the biological chemistry and the physiological roles of the magnesium ion were well known, the regulation of intracellular $Mg^{2+}$ in mammalian cells is not fully understood. More recently, however, the mechanism of $Mg^{2+}$ mobilization by hormonal stimulation has been investigated in hearts and in myocytes. In this work we have investigated the regulation mechanism responsible for the $Mg^{2+}$ mobilization induced by ${\alpha}1-adrenoceptor$ stimulation in perfused guinea pig hearts or isolated myocytes. The $Mg^{2+}$ content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry. The elimination of $Mg^{2+}$ in the medium increased the force of contraction of right ventricular papillary muscles. Phenylephrine also enhanced the force of contraction in the presence of $Mg^{2+}$-free medium. ${\alpha}1-Agonists$ such as phenylephrine were found to induce $Mg^{2+}$ efflux in both perfused hearts or myocytes. This was blocked by prazosin, a ${\alpha}1-adrenoceptor$ antagonist. $Mg^{2+}$ efflux by phenylephrine was amplified by $Na^+$ channel blockers, an increase in extracellular $Ca^{2+}$ or a decrease in extracellular $Na^+$. By contrast, the $Mg^{2+}$ influx was induced by verapamil, nifedipine, ryanodine, lidocaine or tetrodotoxin in perfused hearts, but not in myocytes. $W_7$, a $Ca^{2+}/calmodulin$ antagonist, completely blocked the pheylephrine-, A23187-, veratridine-, $Ca^{2+}-induced$ $Mg^{2+}$ efflux in perfused hearts or isolated myocytes. In addition, $Mg^{2+}$ efflux was induced by $W_7$ in myocytes but not in perfused heart. In conclusion, An increase in $Mg^{2+}$ efflux by ${\alpha}1-adrenoceptor$ stimulation in hearts can be through $IP_3$ and $Ca^{2+}-calmodulin$ dependent mechanism.

기니픽 심장에서 histamine H₂-수용체 자극에 의한 Mg²⁺ 유리에 대한 phosphodiesterase 억제제의 효과

강형섭,김진상,Kang, Hyung-sub,Kim, Jin-shang 대한수의학회 2000 大韓獸醫學會誌 Vol.40 No.3

Several recent studies demonstrate that receptor-mediated cAMP (adenosine 3',5'-monophosphate) production evokes marked change in magnesium ($Mg^{2+}$) homeostasis. The effects of dimaprit or/and phosphodiesterase (PDE) inhibitors on the $Mg^{2+}$ release from perfused guinea pig heart and collagenase-dispersed myocytes was studied to clarify an association of $H_2-histaminergic$ receptor-mediated $Mg^{2+}$ regulation with intracellular cAMP-degradation system. $Mg^{2+}$ efflux was stimulated in perfused hearts and myocytes by IBMX (3-isobutyl-1-methylxanthine), a calmodulin-sensitive PDE inhibitor, but not by RO 20-1724(4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone) or papaverine, cAMP-specific PDE inhibitors. $Mg^{2+}$ efflux was also be induced by dimaprit, a H-2-agonist. $Mg^{2+}$ effluxes induced by dimaprit were augmented by the presence of the PDE inhibitors. The augmentation of dimaprit-induced $Mg^{2+}$ effluxes by the PDE inhibitors were inhibited by ranitidine, a $H_2-antagonist$, and imipramine, a $Na^{+}-Mg^{2+}$ exchange inhibitor, in perfused hearts and myocytes and were also inhibited by amiloride in perfused hearts. These results suggest that the $H_2$-stimulated $Mg^{2+}$ effluxes from guinea pig heart can be regulated by the cytosolic nonspecific-dependent PDE systems and that it is induced by the $Na^{+}-Mg^{2+}$ exchanger stimulation.

Glass ceramic coating on LiNi0.8Co0.1Mn0.1O2 cathode for Li-ion batteries

강형섭,Palanisamy Santhoshkumar,박재우,심규상,MURUGAN NANTHAGOPAL,이창우 한국화학공학회 2020 Korean Journal of Chemical Engineering Vol.37 No.8

Alleviating the surface degradation of Ni-rich cathode materials is desirable to achieve better electrochemical performance. Herein, we report the surface coating of lithium diborate (Li2O-2B2O3) over the Ni-rich LiNi0.8Co0.1Mn0.1O2 (NCM811) cathode material and the systematic investigation of its electrochemical properties. The structural and morphological properties were characterized through X-ray diffraction (XRD), high resolution field-emission scanning electron microscopy (HR FE-SEM), and high resolution field-emission transmission electron microscopy (HR FE-TEM). As a cathode material for Li-ion batteries, the 1.0 wt% Li2O-2B2O3 coated NCM811 exhibits better electrochemical properties than the bare NCM811 as well as 0.5 and 2wt% coated electrodes at room and elevated temperatures (60 oC). The improved electrochemical performance of 1.0 wt% Li2O-2B2O3 coated NCM811 might be due to the optimal coating amount that promotes better ion and electron movement along with prevention of surface degradation.

Effect of Lithium Boron Oxide Coating on Li[Ni_0.8Co_0.1Mn_0.1]O₂ Cathodes for Lithium Ion Batteries

강형섭,이창우 한국공업화학회 2018 한국공업화학회 연구논문 초록집 Vol.2018 No.1