Literature DB >> 6823092

Kinetics of amyloid deposition. II. The effects of dimethylsulfoxide and colchicine therapy.

R Kisilevsky, L Boudreau, D Foster.   

Abstract

Amyloid (AA) protein, when deposition begins, is deposited in two stages--a rapid deposition period of 2 weeks and a plateau stage. The effect of dimethylsulfoxide (DMSO) and colchicine therapy on the kinetics of amyloid deposition was dependent on the stage of the disease at which therapy began. If given during the rapid deposition period, colchicine delayed the increase in amyloid but did not abolish it. Eventually, splenic and liver amyloid reached the level seen in untreated animals. On the other hand, DMSO given during the rapid deposition period led to significant resorption of both splenic and liver amyloid. By contrast, colchicine and DMSO given after the rapid deposition period were essentially without effect in promoting amyloid resorption. These results correlated well with the serum levels of SAA, the putative AA precursor. Colchicine given during the period of rapid AA deposition caused a transient decline in SAA levels, which eventually returned to levels seen in untreated animals. DMSO given during the rapid deposition period rapidly abolished the high SAA levels and maintained it at a level seen in normal animals. Both colchicine and DMSO therapy, if instituted after the rapid amyloid deposition period, failed to reduce SAA levels significantly below that of untreated controls.

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Year:  1983        PMID: 6823092

Source DB:  PubMed          Journal:  Lab Invest        ISSN: 0023-6837            Impact factor:   5.662


  5 in total

1.  In vivo fragmentation of heparan sulfate by heparanase overexpression renders mice resistant to amyloid protein A amyloidosis.

Authors:  Jin-Ping Li; Martha L Escobar Galvis; Feng Gong; Xiao Zhang; Eyal Zcharia; Shula Metzger; Israel Vlodavsky; Robert Kisilevsky; Ulf Lindahl
Journal:  Proc Natl Acad Sci U S A       Date:  2005-04-20       Impact factor: 11.205

2.  Neutrophil association and degradation of normal and acute-phase high-density lipoprotein 3.

Authors:  E G Shephard; F C de Beer; M C de Beer; M S Jeenah; G A Coetzee; D R van der Westhuyzen
Journal:  Biochem J       Date:  1987-12-15       Impact factor: 3.857

3.  Improvement of endoscopic and histologic findings of AA-type gastrointestinal amyloidosis by treatment with dimethyl sulfoxide and prednisolone.

Authors:  A Takahashi; J Matsumoto; S Nishimura; N Tanida; S Imura; T Isobe; T Shimoyama
Journal:  Gastroenterol Jpn       Date:  1985-04

4.  Biochemical nature and cellular origin of amyloid enhancing factor (AEF) as determined by anti-AEF antibody.

Authors:  K Alizadeh-Khiavi; Z Ali-Khan
Journal:  Br J Exp Pathol       Date:  1988-10

5.  Quantitative tomography of early-onset spontaneous AA amyloidosis in interleukin 6 transgenic mice.

Authors:  Jonathan S Wall; Tina Richey; Amy Allen; Robert Donnell; Steve J Kennel; Alan Solomon
Journal:  Comp Med       Date:  2008-12       Impact factor: 0.982

  5 in total

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