Pharmacokinetic and pharmacodynamic interactions of morin and cyclosporin

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Title:	Pharmacokinetic and pharmacodynamic interactions of morin and cyclosporin
Authors:	Fang, SH;Hou, YC;Chao, PDL
Contributors:	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
Date:	2005
Issue Date:	2010-09-24 15:02:59 (UTC+8)
Publisher:	ACADEMIC PRESS INC ELSEVIER SCIENCE
Abstract:	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.
Relation:	TOXICOLOGY AND APPLIED PHARMACOLOGY 205(1):65-70
Appears in Collections:	[School of Medicine] Journal articles

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