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2017 ; 2017
(ä): 5278218
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Kaempferide Protects against Myocardial Ischemia/Reperfusion Injury through
Activation of the PI3K/Akt/GSK-3? Pathway
#MMPMID28928604
Wang D
; Zhang X
; Li D
; Hao W
; Meng F
; Wang B
; Han J
; Zheng Q
Mediators Inflamm
2017[]; 2017
(ä): 5278218
PMID28928604
show ga
The aim of this study is to investigate both the efficacy and mechanism of action
of kaempferide (Kae) as a therapy for the treatment of cardiovascular disease. A
rat model of myocardial ischemia/reperfusion (I/R) injury was established by
ligation of the left anterior descending coronary artery for 30?min followed by a
2?h perfusion. In our study, we show that Kae remarkably improved cardiac
function, alleviated myocardial injury via a decrease in myocardial enzyme
levels, and attenuated myocardial infarct size in a dose-dependent manner. In
addition, preconditioning treatment with Kae was found to significantly decrease
serum TNF-?, IL-6, C-reactive protein (CRP), MDA, and ROS levels, while it was
found to increase serum levels of SOD. Nuclear factor erythroid 2-related factor
2 (Nrf2) and cleaved caspase-3 expression levels were observed to be
downregulated, while phospho-Akt (p-Akt) and phospho-glycogen synthase kinase-3?
(p-GSK-3?) expression levels were upregulated. However, cotreatment with LY294002
(a PI3K inhibitor) or TDZD-8 (a GSK-3? inhibitor) was found to abolish the above
cardioprotective effects observed with the Kae treatment. The data presented in
this study provides evidence that Kae attenuates I/R-induced myocardial injury
through inhibition of the Nrf2 and cleaved caspase-3 signaling pathways via a
PI3K/Akt/GSK 3?-dependent mechanism.
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