Effects of Ghrelin on human alveolar epithelial cell apoptosis in response to lipopolysaccharide through AKT/ERK signaling pathway / 中国免疫学杂志
Chinese Journal of Immunology
;
(12): 1129-1134, 2017.
Artículo
en Chino
| WPRIM
| ID: wpr-608836
ABSTRACT
Objective:
To investigate the protective effects of Ghrelin on LPS-induced apoptosis of human alveolar epithelial A549 cells,along with the possible molecular mechanisms.Methods:
CCK-8 assay was used to examine the cell viability of A549 treated by LPS.Apoptosis of A549 cells was measured by TUNEL.NO(Nitric oxide)production was detected by NO-specific fluorescent probe 3-Amino,4-aminomethyl-2′,7′-difluoresceindiacetate(DAF-FM DA).Western blot was also performed to examine the expressions of iNOS(inducible nitric oxide synthase),AKT,ERK,p-AKT,p-ERK and apoptotic proteins,such as Bcl-2,Bax,and cleaved caspase-3.Results:
LPS exposure impaired cell viability and increased apoptosis of A549 cells significantly in concentration-and time-dependent manners accompanied with increased Bax and cleaved caspase-3 production,coupled with decreased Bcl-2 levels.Meanwhile,LPS promoted iNOS expression and the production of NO.Ghrelin pretreatment ameliorated LPS-caused alterations in the ratio of Bax/Bcl-2 and cleaved caspase-3 expression.TUNEL analysis showed that Ghrelin could decrease the apoptosis induced by LPS in A549(P<0.05).Simultaneously,LPS remarkably decreased the expression of p-AKT and p-ERK in A549 cells,which was abrogated by Ghrelin pretreatment.However,Ghrelin had no significant effect on NO production induced by LPS.Conclusion:
Ghrelin reduces LPS-induced apoptosis of human alveolar epithelial cells partly through activating the AKT and ERK pathway,but the level of iNOS derived NO could not be reduced.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Chinese Journal of Immunology
Año:
2017
Tipo del documento:
Artículo
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