中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/30838
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    題名: Pharmacokinetic and pharmacodynamic interactions of morin and cyclosporin
    作者: Fang, SH;Hou, YC;Chao, PDL
    貢獻者: 醫學院醫學系微生物學科;China Med Univ, Sch Med, Dept Microbiol, Taichung 404, Taiwan;China Med Univ, Sch Chinese Med, Dept Microbiol, Taichung 404, Taiwan;China Med Univ, Sch Pharm, Dept Microbiol, Taichung 404, Taiwan
    日期: 2005
    上傳時間: 2010-09-24 15:02:59 (UTC+8)
    出版者: ACADEMIC PRESS INC ELSEVIER SCIENCE
    摘要: To evaluate the anti-sepsis potential of YC- I, we have examined the effect of YC- I on the regulation of cytokine production in human leukocytes and enclotoxemic mice. The data demonstrated that YC- I showed a preferential inhibition on proinflammatory cytokine production without inhibition of cell growth or induction of cytotoxicity in human leukocytes. On the other hand, in the septic mouse model, treatment with an intraperitoneal application of LPS caused a cumulative death within 27 hours. The post-treatment administration of YC- I significantly increased the survival rate in enclotoxemic mice. Furthermore, several mediators were detected and the data showed that YC- I profoundly blocked LPS-induced NO as well as TNF-α production, and prevented lung damage by histological examination.Samples from the animal model showed that LPS-induced NFκ B/DNA binding activity and consequent up-regulation of iNOS expression in tissues were abolished by post-administration of YC- I. FurthermoreYC- I, by itself,did not modify cGMP content while significantly inhibit LPS-induced cGMP formation, suggesting that YC- I -mediated effect was not through a cGMP-elevating pathway.Taken together, it is evident that the post-treatment administration of YC- I after LPS application significantly inhibits NF-κ B activation, iNOS expression, NO over-production, and cytokine release reaction resulting in an improved survival rate in endotoxemic mice. It is suggested that YC- I may be a potential agent for the therapeutic treatment of sepsis. Samples from the animal model showed that LPS-induced NFκ B/DNA binding activity and consequent up-regulation of iNOS expression in tissues were abolished by post-administration of YC- I. Furthermore, YC- I, by itselfdid not modify cGMP content while significantly inhibit LPS-induced cGMP formation, suggesting that YC- I -mediated effect was not through a cGMP-elevating pathway.Taken together, it is evident that the post-treatment administration of YC- I after LPS application significantly inhibits NF-κ B activation, iNOS expression, NO over-production, and cytokine release reaction resulting in an improved survival rate in enclotoxemic mice. It is suggested that YC- I may be a potential agent for the therapeutic treatment of sepsis.
    關聯: TOXICOLOGY AND APPLIED PHARMACOLOGY 205(1):65-70
    顯示於類別:[醫學系] 期刊論文

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