Icariin ameliorates cisplatin-induced cytotoxicity in human embryonic kidney 293 cells by suppressing ROS-mediated PI3K/Akt pathway.
In: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, Jg. 109 (2019), S. 2309
Online
academicJournal
Zugriff:
Cisplatin, as an effective chemotherapeutic agent, is widely used to treat verious types of cancers. Nephrotoxicity induced by cisplatin seriously limits its clinical application. Icariin, a major and remarkable flavonoid isolated from Epimedium koreanum, has been reported to exert anti-oxidative stress and anti-inflammation actions. The purpose of this study is to explore the protective effect and possible mechanism of icariin on cisplatin-induced nephrotoxicity on HEK-293 cells. In this study, icariin pretreatment for 24 h significantly ameliorated cisplatin-induced oxidative stress by reducing levels of malondialdehyde (MDA) and reactive oxygen species (ROS), while increasing level of glutathione (GSH) in HEK-293 cells. Furthermore, icariin pretreatment reduced NF-κB phosphorylation and nuclear translocation in HEK-293 cells followed by decreased secretion of IL-1β, TNF-α, and iNOS, suggesting a suppression of inflammatory response. Moreover, icariin pretreatment significantly reduced cellular apoptosis via reduced levels of Bax, cleaved caspase-3/9, and increased anti-apoptotic protein Bcl-2 in the cells. Importantly, LY294002, a specific PI3K inhibitor, abrogated the anti-apoptosis effect of icariin, implicating the involvement of PI3K/Akt pathway. In summary, icariin prevents cisplatin-induced HEK-293 cell injury by inhibiting oxidative stress, inflammatory response, and cellular apoptosis partly via regulating NF-κB and PI3K/Akt signaling pathways. Icariin may serve as a potential therapeutic target against cisplatin-induced nephrotoxicity.
(Copyright © 2018. Published by Elsevier Masson SAS.)
Titel: |
Icariin ameliorates cisplatin-induced cytotoxicity in human embryonic kidney 293 cells by suppressing ROS-mediated PI3K/Akt pathway.
|
---|---|
Autor/in / Beteiligte Person: | Zhou, YD ; Hou, JG ; Yang, G ; Jiang, S ; Chen, C ; Wang, Z ; Liu, YY ; Ren, S ; Li, W |
Link: | |
Zeitschrift: | Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, Jg. 109 (2019), S. 2309 |
Veröffentlichung: | Paris : Editions Scientifiques Elsevier ; <i>Original Publication</i>: New York, N.Y. : Masson Pub. USA, Inc., c1982-, 2019 |
Medientyp: | academicJournal |
ISSN: | 1950-6007 (electronic) |
DOI: | 10.1016/j.biopha.2018.11.108 |
Schlagwort: |
|
Sonstiges: |
|