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2017 ; 2017
(ä): 2869405
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Relaxin Attenuates Contrast-Induced Human Proximal Tubular Epithelial Cell
Apoptosis by Activation of the PI3K/Akt Signaling Pathway In Vitro
#MMPMID28540295
Xie XC
; Cao Y
; Yang X
; Xu QH
; Wei W
; Wang M
Biomed Res Int
2017[]; 2017
(ä): 2869405
PMID28540295
show ga
Background. Contrast-induced acute kidney injury (CI-AKI) is one of the main
causes of iatrogenic acute kidney injury (AKI); however, therapeutic strategies
for AKI remain limited. This study aims to explore the effect of relaxin (RLX) on
contrast-induced HK-2 apoptosis and its underlying mechanisms. Methods. Renal
tubular epithelial cells (HK-2) were incubated either with or without ioversol,
human H2 relaxin, and LY294002 (the inhibitor of the PI3K/Akt signal pathway).
Cell viability was evaluated with a CCK-8 assay. Apoptotic morphologic
alterations were observed using the Hoechst 33342 staining method. Apoptosis was
detected with Annexin V staining. Western blot analysis was employed to measure
the expression of pAkt (S473), Akt, cleaved caspase-3, Bcl-2, Bax, and actin
proteins. Results. Ioversol reduced the viability of HK-2 cells. Western blotting
results revealed decreased expression of phosphorylated Akt in cells treated with
ioversol. The activities of caspase-3 and Bax protein increased, while the
expression of Bcl-2 protein decreased. As a result, the Bax/Bcl-2 ratio increased
after treatment with ioversol. These effects were reversed when HK-2 cells were
cotreated with RLX. However, with preadministration of PI3K/Akt pathway inhibitor
LY294002, the effect of RLX was blocked. Conclusion. Our study demonstrates that
relaxin attenuates ioversol induced cell apoptosis via activation of the PI3K/Akt
signaling pathway, suggesting that RLX might play a protective role in the
treatment of CI-AKI.