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Endothelin-1에 의한 phospholipase C 활성화와 세포내 Ca2+ 이동에 미치는 protein kinase 들의 효과
조중형(Jung Hyung Cho),김현준(Hyun Jun Kim),이윤혜(Yun Hye Lee),박진형(Jin Hyoung Park),장용운(Youn Un Jang),이승준(Seung June Lee),이준한(June Han Lee),윤정이(Jeong Yi Yoon),김창종(Chang Jong Kim),심상수(Sang Soo Sim) 대한약학회 2000 약학회지 Vol.44 No.2
To investigate the effects of protein kinases on endothelin-l-induced phospholipase C activation and Ca2+ mobilization in Rat-2 fibroblast, we measured the formation of inositol phosphates and intracellular Ca2+ concentration with [3H]inositol and Fura-2/AM, respectively. Endothelin-1 dose-dependently activated phospholipase C and increased intracellular Ca2+ concentration. Protein kinase C activator, PMA, significantly inhibited both phospholipase C activity and Ca2+ mobilization induced by endothelin-1. Tyrosine kinase inhibitor, genistein, inhibited both. On the other hand, cyclic nucleotide (cAMP and cGMP) did not have any influence on the signaling pathway of phospholipase C-Ca2+ mobilization induced by endothelin-1. These results suggest that protein kinase C and tyrosine kinase counteract on the signaling pathway of phospholipase C-Ca2+ mobilization induced by endothelin-1 in Rat-2 fibroblast.
KCl과 phenylephrine에 의한 대동맥 수축에서 Ca2+ 길항제와 protein kinase 억제제들의 비교 효과
심상수(Sang Soo Sim),문성원(Sung Won Moon),이윤혜(Yun Hye Lee),이정근(Jung Keun Lee),김현준(Hyun Jun Kim),박진형(Jin Hyoung Park),이준한(June Han Lee),조중형(Jung Hyung Cho),김창종(Chang Jong Kim) 대한약학회 1999 약학회지 Vol.43 No.5
To investigate the difference of contractile mechanism between KCl and phenylephrine-induced contraction, we observed effects of Ca2+ antagonists and protein kinase inhibitors on aorta contraction of rats. Verapamil dose-dependently inhibited the contraction induced by KCl and pheylephrine, the inhibitory effect of verapamil was more potent in KCl-induced contraction than phenylephrine-induced contraction. Econazole and TMB-8 significantly inhibited KCl-induced contraction but did not inhibit phenylephrine-induced contraction. Staurosporine dose-dependently inhibited both KCl and phenylephrine-induced contraction. Genistein and calmodulin antagonists (W-7 and trifluoperazine) also inhibited both contraction in a dose dependent manner. However, the inhibitory effects of genistein and calmodulin antagonists were more potent in pheylephrine-induced contraction than KCl-induced contraction. These results suggest that involvements of Ca2+ channel and protein kinase in rat aorta contraction were dependent on agonist causing aort smooth muscle contraction.
위 평활근에서 수용성 이완에 관여하는 cyclic nucleotide들의 작용
심상수,최현호,이정근,문성원,이준한,조중형,김창종 중앙대학교 약학연구소 1998 약학 논총 Vol.12 No.-
To investigate the actions of cyclic nucleotides associated with receptive relaxation, smooth muscle strips isolated from cat stomach were used to measure the isometric contraction in an isolated organ bath. Both sodium nitroprusside and forskolin inhibited acetylcholine-induced contraction dose-dependently. The inhibitory effect of sodium nitroprusside was more potent than that of forskolin. Verapamil, voltage-dependent calcium channel blocker, and TMB-8, a blocker of intracellular Ca^2+ release, significantly inhibited acetylcholine-induced contraction. Combined effects of verapamil and TMB-8 with sodium nitroprusside (0.1 μM) were significantly greater than that of each one, whereas those with forskolin (1 μM) were similar to that of each one. Tyrosine phosphatase inhibitor, vanadate (10 μM) significantly blocked the inhibitory effects of verapamil (1 μM), TMB -8 (1 μM) and forskolin (1 μM), but did not that of sodium nitroprusside (0.1 μM). However, protein kinase C activator, PMA (10 μM), did not affect the inhibitory effects of the above four agents. From the above results, it is suggested that the action of cAMP on receptive relaxation may be different from that of cGMP, which is modulated by tyrosine phosphatase in gastric smooth muscle.