In:
Pharmacology, S. Karger AG, Vol. 91, No. 3-4 ( 2013), p. 123-130
Abstract:
〈 b 〉 〈 i 〉 Aims: 〈 /i 〉 〈 /b 〉 The association between diabetes and neointimal expansion after vascular injury has been attributed to the accumulation of advanced glycation end products (AGEs). Here we investigated the inhibitory effect of cariporide, a specific Na 〈 sup 〉 + 〈 /sup 〉 /H 〈 sup 〉 + 〈 /sup 〉 exchanger 1 blocker, on neointimal proliferation induced by AGEs in a balloon injury model. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase (MMP) was monitored by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. The level of reactive oxygen species (ROS) was determined by specific fluorescent probe. The phosphorylation of the nuclear factor- & #x0138;B (NF- & #x0138;B) system was studied by Western blot. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Cariporide significantly suppressed AGE-induced neointimal hyperplasia, vascular smooth muscle cell (VSMC) proliferation, COX-2, MMP-2 and MMP-9 expression. In addition, cariporide decreased AGE-induced ROS, malondiadehyde level and increased the superoxide dismutase and glutathione peroxidase activity. We also found that cariporide blocked AGE-induced NF- & #x0138;B activation and inhibitor- & #x0138;B degradation. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The results indicated that cariporide inhibited AGE-induced neointimal formation by suppressing the VSMC proliferation and the up-regulation of COX-2, MMP-2, MMP-9 via inhibiting ROS and NF- & #x0138;B activation.
Type of Medium:
Online Resource
ISSN:
0031-7012
,
1423-0313
Language:
English
Publisher:
S. Karger AG
Publication Date:
2013
detail.hit.zdb_id:
1483550-2
SSG:
15,3
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