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2017 ; 14
(3
): 2613-2618
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Bindarit reduces the incidence of acute aortic dissection complicated lung injury
via modulating NF-?B pathway
#MMPMID28962202
Wu Z
; Chang J
; Ren W
; Hu Z
; Li B
; Liu H
Exp Ther Med
2017[Sep]; 14
(3
): 2613-2618
PMID28962202
show ga
The pathogenesis of acute aortic dissection (AAD) complicated acute lung injury
(ALI) is not currently well defined. At present, no effective animal model has
been established for AAD complicated ALI, which hinders research and development
of an appropriate treatment regimen for the concurrent conditions. The aim of the
present study was to evaluate the therapeutic effects of bindarit (Bnd), an
indazolic derivative, on the production of monocyte chemoattractant protein
(MCP)-1 in angiotensin II (AngII)-induced complicated ALI in rats. An AAD
complicated ALI rat model was established using aminopropionitrile (BAPN) and
AngII. The pathological features of AAD complicated ALI were assessed via
biochemical and histopathological evaluations. AngII-stimulated human pulmonary
microvascular endothelial cells (hPMVECs) were used to assess the effects of Bnd
on MCP-1 expression. Western blot analysis was performed to analyze the
expression of proteins that may be associated with the process. AAD complicated
ALI was established following BAPN and AngII interference, and a massive
accumulation of macrophages was observed in the lung tissues of the study rats.
Bnd was able to significantly attenuate the incidence of AAD complicated ALI
(P<0.05), and significantly inhibit the accumulation of macrophages (P<0.05). The
overexpression of MCP-1 induced by AngII in hPMVECs was significantly inhibited
by Bnd (P<0.05), which may be associated with downregulation of the classical
nuclear factor-?B pathway. Bnd was able to attenuate the incidence of AAD
complicated ALI, and inhibit the accumulation of macrophages in vivo. These
findings provide a basis for future applications of Bnd as part of a therapeutic
treatment schedule for aortic dissection complicated lung injury.
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