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Dexmedetomidine-Induced Contraction Involves CPI-17 Phosphorylation in Isolated Rat Aortas
Ok, Seong-Ho,Kwon, Seong-Chun,Baik, Jiseok,Hong, Jeong-Min,Oh, Jiah,Han, Jeong Yeol,Sohn, Ju-Tae MDPI AG 2016 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.17 No.10
<P>Dexmedetomidine, a highly selective α-2 adrenoceptor agonist, produces vasoconstriction, which leads to transiently increased blood pressure. The goal of this study was to investigate specific protein kinases and the associated cellular signal pathways responsible for the increased calcium sensitization induced by dexmedetomidine in isolated rat aortas, with a particular focus on phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17). The effect of Y-27632 and chelerythrine on the dexmedetomidine-induced intracellular calcium concentration ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) and tension were assessed using fura-2-loaded aortic strips. The effects of rauwolscine, Y-27632, chelerythrine, and ML-7 hydrochloride on the dexmedetomidine-induced phosphorylation of CPI-17 or of the 20-kDa regulatory light chain of myosin (MLC<SUB>20</SUB>) were investigated in rat aortic vascular smooth muscle cells. The effects of rauwolscine, Y-27632, and chelerythrine on the membrane translocation of Rho-kinase and protein kinase C (PKC) phosphorylation induced by dexmedetomidine were assessed. Y-27632 and chelerythrine each reduced the slopes of the [Ca<SUP>2+</SUP>]<SUB>i</SUB>-tension curves of dexmedetomidine-induced contraction, and Y-27632 more strongly reduced these slopes than did chelerythrine. Rauwolscine, Y-27632, chelerythrine, and ML-7 hydrochloride attenuated the dexmedetomidine-induced phosphorylation of CPI-17 and MLC<SUB>20</SUB>. Taken together, these results suggest that dexmedetomidine-induced contraction involves calcium sensitization, which appears to be mediated by CPI-17 phosphorylation via Rho-kinase or PKC.</P>
Biological Activity of Water Extract from Atractylodes macrocephala
Chun Ju Yeon,Lee Hyun Ok,Baek Seung Hwa The Physiological Society of Korean Medicine and T 2004 동의생리병리학회지 Vol.18 No.2
The effects of water extract from Atractylodes macrocephala Koidz on biological activity were investigated. The crude water extract of A. macrocephala inhibited the growth of the dermatophytic fungus Trichophyton mentagrophytes ATCC 28185, (3 mm inhibition zone at 300 ㎍/disc). However, it did not show growth inhibition activity against Sreptococcus mutans JC-2 (MIC >1,000 ㎍/mL). This extract was cytotoxic to P388 murine leukaemia cells ATCC CCL 46 P388D1, (IC/sub 50/ 62.24 ㎍/mL at 150 ㎍/disc). These results suggest that water extract of A. macrocephala possesses antitumoral, and antimicrobial activities.
Ok, Seong-Ho,Lee, Soo Hee,Kwon, Seong-Chun,Choi, Mun Hwan,Shin, Il-Woo,Kang, Sebin,Park, Miyeong,Hong, Jeong-Min,Sohn, Ju-Tae MDPI AG 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.2
<P>The goal of this in vitro study was to examine the effect of a lipid emulsion on toxic-dose bupivacaine-induced vasodilation in a model of tyrosine phosphatase inhibitor sodium orthovanadate-induced contraction in endothelium-denuded rat aortae and to elucidate the associated cellular mechanism. The effect of a lipid emulsion on vasodilation induced by a toxic dose of a local anesthetic during sodium orthovanadate-induced contraction was examined. In addition, the effects of various inhibitors, either bupivacaine alone or a lipid emulsion plus bupivacaine, on protein kinase phosphorylation induced by sodium orthovanadate in rat aortic vascular smooth muscle cells was examined. A lipid emulsion reversed the vasodilation induced by bupivacaine during sodium orthovanadate-induced contraction. The lipid emulsion attenuated the bupivacaine-mediated inhibition of the sodium orthovanadate-induced phosphorylation of protein tyrosine, c-Jun NH<SUB>2</SUB>-terminal kinase (JNK), myosin phosphatase target subunit 1 (MYPT1), phospholipase C (PLC) γ-1 and extracellular signal-regulated kinase (ERK). These results suggest that a lipid emulsion reverses toxic-dose bupivacaine-induced vasodilation during sodium orthovanadate-induced contraction via the activation of a pathway involving either tyrosine kinase, JNK, Rho-kinase and MYPT1 or tyrosine kinase, PLC γ-1 and ERK, and this reversal is associated with the lipid solubility of the local anesthetic and the induction of calcium sensitization.</P>