Multiple Targets of 3-Dehydroxyceanothetric Acid 2-Methyl Ester to Protect Against Cisplatin-Induced Cytotoxicity in Kidney Epithelial LLC-PK1 Cells
- Authors
- Lee, Dahae; Kim, Ki Hyun; Lee, Won Yung; Kim, Chang-Eop; Sung, Sang Hyun; Kang, Kyo Bin; Kang, Ki Sung
- Issue Date
- 1-Mar-2019
- Publisher
- MDPI
- Keywords
- cisplatin; MAPKs; nephrotoxicity; apoptosis
- Citation
- MOLECULES, v.24, no.5
- Journal Title
- MOLECULES
- Volume
- 24
- Number
- 5
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/1742
- DOI
- 10.3390/molecules24050878
- ISSN
- 1420-3049
- Abstract
- Chronic exposure to cisplatin, a potent anticancer drug, causes irreversible kidney damage. In this study, we investigated the protective effect and mechanism of nine lupane- and ceanothane-type triterpenoids isolated from jujube (Ziziphus jujuba Mill., Rhamnaceae) on cisplatin-induced damage to kidney epithelial LLC-PK1 cells via mitogen-activated protein kinase (MAPK) and apoptosis pathways. Cisplatin-induced LLC-PK1 cell death was most significantly reduced following treatment with 3-dehydroxyceanothetric acid 2-methyl ester (3DC2ME). Additionally, apoptotic cell death was significantly reduced. Expression of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 was markedly suppressed by 3DC2ME, indicating inhibition of the MAPK pathway. Treatment with 3DC2ME also significantly reduced expression of active caspase-8 and -3, Bcl-2-associated X protein (Bax), and B cell lymphoma 2 (Bcl-2), indicating the inhibition of apoptosis pathways in the kidneys. We also applied the network pharmacological analysis and identified multiple targets of 3DC2ME related to MAPK signaling pathway and apoptosis.
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