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Effects of cyclosporin and FK-506 on glomerular mesangial cells. Evidence for direct inhibition of thromboxane synthase by low cyclosporin concentrations.

Abstract：

:The cellular sources or molecular mechanisms responsible for the derangement of vasoactive prostanoid levels during immunosuppressive cyclosporin (CSA) therapy have not been defined. Using cultured rat glomerular mesangial cells (MC), the cytostatic, cytotoxic and prostanoid synthesis modulating effects of CSA and FK-506 have been measured and compared with the immunosuppressive action of these drugs. Both, CSA and FK-506 inhibited proliferation of MC at similar doses (IC50 approximately 1 microgram.ml-1). Lymphoproliferation was suppressed with IC50s of 50 ng.ml-1 and < 1 ng.ml-1, respectively. In contrast, and unlike FK-506, CSA caused mesangiolysis (IC50 = 4.5 micrograms.ml-1) and concentration dependently inhibited the interleukin-1 beta (IL-1 beta) stimulated mesangial cell release of TXB2 at nanomolar doses (IC50 = 50 ng.ml-1). In kinetic experiments (6-48 h), CSA 1 ng.ml-1 partially and 1 microgram.ml-1 completely abolished the IL-1 beta augmented mesangial secretion TXB2 at all the time points tested. Both, low and high doses of CSA reduced PGE2 release by only 20-40% and then not until at least 24 h of incubation. Measuring enzymatic capacity of membrane fractions of MC to generate TXB2 or PGE2 from added arachidonic acid (10(-5) M), CSA (0.1-1000 ng.ml-1) caused a dose dependent reduction in cyclooxygenase (COX)/thromboxane synthase activity up to 76%, while PGE2 synthesis (COX/prostaglandin synthase) was decreased by 34%. Immunoblots with a specific COX-1 antiserum revealed that COX-1 protein expression of MC was not affected by CSA.(ABSTRACT TRUNCATED AT 250 WORDS)

journal_name

Eur J Clin Pharmacol

journal_title

European journal of clinical pharmacology

authors

Radeke HH,Kuster S,Kaever V,Resch K

doi

10.1007/BF01428385

subject

Has Abstract

pub_date

1993-01-01 00:00:00

pages

S11-6

eissn

0031-6970

issn

1432-1041

journal_volume

44 Suppl 1

pub_type

杂志文章

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