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高速液體크로마토그라프法에 의한 錠劑 중 Strychnine Nitrate 및 Yohimbine Hydrochloride 의 同時定量
李允中,曺正吉,李東宣,丁海秀 成均館大學校 科學技術硏究所 1987 論文集 Vol.38 No.1
A simple, rapid extraction and simultaneous determination for yohimbine hydrochloride and strychnine nitrate in tablets, using high performance liquid chromatography with a reverse-phase solvent system, is described. Samples were extracted with 50% methanol by sonication. The extracts were filtrated and applied to HPLC. HPLCs of yohimbine hydrochloride and strychnine nitrate were carried out on μ-Bondapak C_18 Radial-pak cartridge(8mm i.d. x 10 cm) and CH_3CN/H_2O/CH_3COOH=20/78/2 for the solvent system. Recoveries from model preparations were more than 98%. This method was considered to be useful for the determination of yohimbine hydrochloride and strychnine nitrate in tablets at the same time.
Pharmacological and electrophysiological characterization of rat P2X currents
Hai Ying Li,Seog Bae Oh,Joong Soo Kim The Korean Academy of Oral Biology 2008 International Journal of Oral Biology Vol.33 No.1
Adenosine 5’-triphosphate (ATP) is an important extracellular signaling molecule which is involved in a variety of physiological responses in many different tissues and cell types, by acting at P2 receptors, either ionotropic (P2X) or G protein-coupled metabotropic receptors (P2Y). P2X receptors have seven isoforms designated as P2X1-P2X7. In this study, we investigated the electrophysiological and pharmacological properties of rat P2X1-P2X4 currents by using whole-cell patch clamp technique in a heterologous expression system. When ATP-induced currents were analyzed in human embryonic kidney (HEK293) cells following transient transfection of rat P2X1-P2X4, the currents showed different pharmacological and electrophysiological properties. ATP evoked inward currents with fast activation and fast desensitization in P2X1- or P2X3- expressing HEK293 cells, but in P2X2- or P2X4-expressing HEK293 cells, ATP evoked inward currents with slow activation and slow desensitization. While PPADS and suramin inhibited P2X2 or P2X3 receptor-mediated currents, they had little effects on P2X4 receptor-mediated currents. Ivermectin potentiated and prolonged P2X4 receptor-mediated currents, but did not affect P2X2 or P2X3 receptor-mediated currents. We suggest that distinct pharmacological and electrophysiological properties among P2X receptor subtypes would be a useful tool to determine expression patterns of P2X receptors in the nervous system including trigeminal sensory neurons and microglia.
Eugenol Inhibits ATP-induced P2X Currents in Trigeminal Ganglion Neurons
Hai Ying Li,Byung Ky Lee,Joong Soo Kim,Sung Jun Jung,Seog Bae Oh 대한생리학회-대한약리학회 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.6
Eugenol is widely used in dentistry to relieve pain. We have recently demonstrated voltage-gated Na<sup>+</sup> and Ca<sup>2+</sup> channels as molecular targets for its analgesic effects, and hypothesized that eugenol acts on P2X<sub>3</sub>, another pain receptor expressed in trigeminal ganglion (TG), and tested the effects of eugenol by whole-cell patch clamp and Ca<sup>2+</sup> imaging techniques. In the present study, we investigated whether eugenol would modulate 5 -triphosphate (ATP)-induced currents in rat TG neurons and P2X<sub>3</sub>-expressing human embryonic kidney (HEK) 293 cells. ATP-induced currents in TG neurons exhibited electrophysiological properties similar to those in HEK293 cells, and both ATP- and Ձ,Ղ-meATP-induced currents in TG neurons were effectively blocked by TNP-ATP, suggesting that P2X<sub>3</sub> mediates the majority of ATP-induced currents in TG neurons. Eugenol inhibited ATP-induced currents in both capsaicin-sensitive and capsaicin-insensitive TG neurons with similar extent, and most ATP-responsive neurons were IB4-positive. Eugenol inhibited not only Ca<sup>2+</sup> transients evoked by Ձ,Ղ-meATP, the selective P2X<sub>3</sub> agonist, in capsaicin-insensitive TG neurons, but also ATP-induced currents in P2X<sub>3</sub>-expressing HEK293 cells without co-expression of transient receptor potential vanilloid 1 (TRPV1). We suggest, therefore, that eugenol inhibits P2X<sub>3</sub> currents in a TRPV1-independent manner, which contributes to its analgesic effect.
Joong Won Lee,Yang Jee Kim,Young Joo Choi,Hae Dong Woo,Gye Eun Kim,Tae Kyung Ha,Young Hyun Lee,Hai Won Chung 한국독성학회 2009 Toxicological Research Vol.25 No.4
Uncontrolled cell growth and increased cell proliferation are major features of cancer that are dependent on the stable structure and dynamics of the cytoskeleton. Since stable cytoskeleton structure and dynamics are partly regulated by myosin light chain kinase (MLCK), many current studies focused on MLCK inhibition as a chemotherapeutic target. As a potent and selective MLCK inhibitor, ML-7 [1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazapine hydrochloride] is a promising candidate for an anticancer agent, which would induce apoptosis as well as prevents invasion and metastasis in certain types of cancer cells. This study assessed cytotoxic effects of ML-7 against HL-60 cells and therapeutic efficacy of ML-7 as a potential antileukemia agent. Trypan-blue exclusion assays showed dose- and time- dependent decreases in ML-7 treated HL-60 cells (p < 0.05). Comet assays revealed a significant increase in DNA damage in HL-60 cells after treatment with 40 μM ML-7 for 2 h. Sub-G1 fractions, analyzed by flow cytometry increased in a dose-dependent manner, suggesting that ML-7 can induce apoptotic cell death in HL-60 cells. ML-7 was selectively cytotoxic towards HL-60 cells; not affecting normal human lymphocytes. That selective effect makes it a promising potential anti-leukemia agent. In addition, anticancer efficacy of ML-7 in combination with flavonoids (genistein or quercetin) or anticancer drugs (cisplatin or Ara-C) against HL-60 cells was assessed. Combination of ML-7 with flavonoids increased the anti-cancer effect of ML-7 to a greater extent than combination with the anticancer drugs. This implies that ML-7 in combination with flavonoids could increase the efficacy of anticancer treatment, while avoiding side effects cansed by conventional anticancer drug-containing combination chemotherapy.
Lee, Joong-Won,Kim, Yang-Jee,Choi, Young-Joo,Woo, Hae-Dong,Kim, Gye-Eun,Ha, Tae-Kyung,Lee, Young-Hyun,Chung, Hai-Won Korean Society of ToxicologyKorea Environmental Mu 2009 Toxicological Research Vol.26 No.4
Uncontrolled cell growth and increased cell proliferation are major features of cancer that are dependent on the stable structure and dynamics of the cytoskeleton. Since stable cytoskeleton structure and dynamics are partly regulated by myosin light chain kinase (MLCK), many current studies focused on MLCK inhibition as a chemotherapeutic target. As a potent and selective MLCK inhibitor, ML-7 [1-(5-iodonaphthalene-1-sulfonyl)-1 H-hexahydro-1,4-diazapine hydrochloride] is a promising candidate for an anticancer agent, which would induce apoptosis as well as prevents invasion and metastasis in certain types of cancer cells. This study assessed cytotoxic effects of ML-7 against HL-60 cells and therapeutic efficacy of ML-7 as a potential antileukemia agent. Trypan-blue exclusion assays showed dose- and time- dependent decreases in ML-7 treated HL-60 cells (p<0.05). Comet assays revealed a significant increase in DNA damage in HL-60 cells after treatment with $40{\mu}M$ ML-7 for 2h. Sub-G1 fractions, analyzed by flow cytometry increased in a dose-dependent manner, suggesting that ML-7 can induce apoptotic cell death in HL-60 cells. ML-7 was selectively cytotoxic towards HL-60 cells; not affecting normal human lymphocytes. That selective effect makes it a promising potential anti-leukemia agent. In addition, anticancer efficacy of ML-7 in combination with flavonoids (genistein or quercetin) or anticancer drugs (cisplatin or Ara-C) against HL-60 cells was assessed. Combination of ML-7 with flavonoids increased the anti-cancer effect of ML-7 to a greater extent than combination with the anticancer drugs. This implies that ML-7 in combination with flavonoids could increase the efficacy of anticancer treatment, while avoiding side effects cansed by conventional anticancer drug-containing combination chemotherapy.