Familial amyloidosis in one Chinese family: Clinical, immunological, and molecular genetic analysis

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Title:	Familial amyloidosis in one Chinese family: Clinical, immunological, and molecular genetic analysis
Authors:	Chou, CT;Lee, CC;Chang, DM;Buxbaum, JN;Jacobson, DR
Contributors:	附設醫院經經部;CHINA MED COLL HOSP,DEPT NEUROL,TAICHUNG,TAIWAN;TRI SERV GEN HOSP,DEPT MED,TAIPEI,TAIWAN;NEW YORK DEPT VET AFFAIRS MED CTR,MED SERV,NEW YORK,NY;NEW YORK DEPT VET AFFAIRS MED CTR,RES SERV,NEW YORK,NY;NYU,SCH MED,NEW YORK,NY
Date:	1997
Issue Date:	2010-09-24 14:51:45 (UTC+8)
Publisher:	BLACKWELL SCIENCE LTD
Abstract:	In rat neutrophils, formylmethionyl-leucyl-phenylalanine (fMLP)-induced inositol phosphate formation was concentration-dependently inhibited by acetylshikonin as well as by a putative phospholipase C (PLC) inhibitor [6-[[17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122). The IC50 value of acetylshikonin for the inhibition of inositol trisphosphate (IP3) formation was estimated to be 16.1 +/- 1.5 mu M. The reduction of inositol phosphate levels appeared to reflect inhibition of PLC activity because the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) catalyzed by a soluble fraction from neutrophils was also inhibited by acetylshikonin (IC50 value 21.4 +/- 6.1 mu M) over the same range of concentrations. Although acetylshikonin alone evoked Ca2+ and Mn2+ influx into neutrophils in Ca2+-containing medium, acetylshikonin, like U73122, inhibited Ca2+ release (IC50 value similar to 5.3 +/- 0.4 mu M) from internal stores in Ca2+-free medium. These results indicate that acetylshikonin inhibits phosphatidylinositol signaling in neutrophils. (C) 1997 Elsevier Science Inc.
Relation:	JOURNAL OF INTERNAL MEDICINE 241(4):327-331
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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