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Two New Acorane Sesquiterpenes from Illicium henryi
Tai-Fa Song,Wei-Dong Zhang,Xin-Hua Xia,Yun-Heng Shen,Chun-Mei Liu,Sheng Lin,Hui-zi Jin,Hui-Liang Li 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.9
Two new acorane sesquiterpenes, 10-hydroxyacoronene (1) and 1β-isopropyl-4β-methyl-9β-hydroxy spiro[4.5]dec-6-en-8-one (2), one new natural product, 4-hydroxy-4, 6-dimethyl-1-tetralone (3), and one known acorane sesquiterpene, acoradiepoxide (4) were isolated from the twigs and leaves of Illicium henryi. The structures of the new compounds were elucidated primarily on the basis of analysis of spectroscopic data. In addition, the inhibitory effect on NO production of these compounds were tested. Compounds 1 and 4 exhibited slight inhibitory effects on NO production with IC50 values of 82.4 μg/mL and 76.5 μg/mL, respectively.
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Sphingosine 1-Phosphate-induced Signal Transduction in Cat Esophagus Smooth Muscle Cells
Hyun Ju Song,Tai Sik Choi,Fa Yong Chung,박선영,Jung Soo Ryu,Jae Gwang Woo,민영실,Chang Yell Shin,손의동 한국분자세포생물학회 2006 Molecules and cells Vol.21 No.1
We investigated the mechanism of contraction induced by S1P in esophageal smooth muscle cells. Western blot analysis demonstrated that S1P1, S1P2, S1P3, and S1P5 receptors existed in the cat esophagus. Only penetration of EDG-5 (S1P2) antibody into permeabilized cells inhibited S1P-induced contraction. Pertussis toxin (PTX) also inhibited contraction, suggesting that it was mediated by S1P2 receptors coupled to a PTXsensitive Gi protein. Specific antibodies to Gi2, Gq and Gβ inhibited contraction, implying that the S1Pinduced contraction depends on PTX-insensitive Gq and Gβ dimers as well as the PTX-sensitive Gi2. Contraction was not affected by the phospholipase A2 inhibitor DEDA, or the PLD inhibitor ρ-chloromercuribenzoate, but it was abolished by the PLC inhibitor U73122. Incubation of permeabilized cells with PLCβ3 antibody also inhibited contraction. Contraction involved the activation of a PKC pathway since it was affected by GF109203X and chelerythrine. Since PKCε antibody inhibited contraction, PKCε may be required. Preincubation of the muscle cells with the MEK inhibitor PD98059 blocked S1P-induced contraction, but the p38 MAP kinase inhibitor SB202190 did not. In addition, co-treatment of cells with GF 109203X and PD98059 did not have a synergistic effect, suggesting that these two kinases are involved in the same signaling pathway. Our data suggest that S1P-induced contraction in esophageal smooth muscle cells is mediated by S1P2 receptors coupled to PTXsensitive Gi2 proteins, and PTX-insensitive Gq and Gβ proteins, and that the resulting activation of the PLCβ3 and PKCε pathway leads to activation of a p44/p42 MAPK pathway.
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