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2016 ; 6
(ä): 21992
Nephropedia Template TP
Tian F
; Yao J
; Yan M
; Sun X
; Wang W
; Gao W
; Tian Z
; Guo S
; Dong Z
; Li B
; Gao T
; Shan P
; Liu B
; Wang H
; Cheng J
; Gao Q
; Zhang Z
; Cao W
; Tian Y
Sci Rep
2016[Feb]; 6
(ä): 21992
PMID26911899
show ga
Necroptosis, or programmed necrosis, contributes to the formation of necrotic
cores in atherosclerotic plaque in animal models. However, whether inhibition of
necroptosis ameliorates atherosclerosis is largely unknown. In this study, we
demonstrated that necroptosis occurred in clinical atherosclerotic samples,
suggesting that it may also play an important role in human atherosclerosis. We
established an in vitro necroptotic model in which necroptosis was induced in
THP-1-derived foam cells by serum deprivation. With this model, we demonstrated
that 5-aminolevulinic acid-mediated sonodynamic therapy (ALA-SDT) inhibited
necroptosis while promoting apoptosis. ALA-SDT activated the caspase-3 and
caspase-8 pathways in foam cells, which is responsible for the switch from
necroptosis to apoptosis. The inhibition of either caspase-8 or caspase-3
abolished the anti-necroptotic effect of ALA-SDT. In addition, we found that
caspase-3 activation peaked 4?hours after ALA-SDT treatment, 2?hours earlier than
maximal caspase-8activation. Taken together, our data indicate that ALA-SDT
mediates the switch from necroptosis to apoptosis by activating the caspase-3 and
caspase-8 pathways and may improve the prognosis of atherosclerosis.