Dipyridamole抑制高糖透析液促進腹膜纖維化之作用機轉
Date Issued
2002
Date
2002
Author(s)
洪冠予
DOI
902314B002272
Abstract
High glucose (HG) contents of dialysate exerts fibrogenic effects on peritoneum of
patients on peritoneal dialysis (PD). We previously had found in human peritoneal
mesothelial cell (HPMC) that the fibrogenic effect of TGF-ß was mediated via activation of
extracellular signal-regulated kinase (ERK) cascade and is suppressed by dipyridamole.
However, the molecular mechanisms mediating fibrogenic reactions of HG in HPMC and
whether it can be modulated by dipyridamole has never been investigated. HG (25 mM),
compared with normal glucose (5.5 mM), significantly activate ERK1/2, p38 MAPK and
increased type I pro-collagen [proá1(I)] mRNA level in HPMC. HPMC pre-treated with
dipyridamole dose-dependently inhibit effects of HG. HPMC pre-treated with PD98059 and
SB203580, which selectively inhibited ERK and p38 MAPK, respectively, prevented
HG-induced proá1(I) mRNA upregulation. It implicated that both ERK and p38 MAPK are
involved in response to HG. Dipyridamole inhibited the ERK activation, but not the activation
of p38 MAPK, of HPMC by HG. We postulated that dipyridamole may inhibit the
HG-induced matrix gene expression, thus may have clinical implications as therapeutic agents
for prevention of peritoneal fibrosising syndrome (PFS).
Subjects
peritoneal dialysis
mesothelial cell
high glucose
signal transduction
Publisher
臺北市：國立臺灣大學醫學院內科
Type
report
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