Anti-apoptotic and antioxidant effects of 3-epi-iso- seco-tanapartholide isolated from artemisia argyi against iodixanol-induced kidney epithelial cell death
- Authors
- Lee D.; Kim K.O.; Lee D.; Kang K.S.
- Issue Date
- Jun-2020
- Publisher
- MDPI AG
- Keywords
- Apoptosis; Contrast agent; Cytotoxicity; Iodixanol; Oxidative stress
- Citation
- Biomolecules, v.10, no.6, pp.1 - 18
- Journal Title
- Biomolecules
- Volume
- 10
- Number
- 6
- Start Page
- 1
- End Page
- 18
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/76192
- DOI
- 10.3390/biom10060867
- ISSN
- 2218-273X
- Abstract
- Iodixanol is a non-ionic iso-osmolar contrast agent, but it is a risk factor for kidney damage and increases morbidity and mortality. In this study, we investigated the effect of 9 sesquiterpenes isolated from mugwort (Artemisia argyi) in contrast agent-induced cytotoxicity in LLC-PK1 cells. Cells were exposed to nine sesquiterpene compounds for 2 h, followed by incubation with iodixanol for 3 h. Cell viability was assessed using the Ez-Cytox assay. The level of reactive oxygen species was measured using 2′,7′-dichlorodihydrofluorescein diacetate staining. Apoptotic cell death was detected using annexin V/PI staining. In addition, immunofluorescence staining and western blotting were performed using antibodies against proteins related to apoptosis, oxidative stress, and MAPK pathways. The most effective 3-epi-iso-seco-tanapartholide (compound 8) among the 9 sesquiterpene compounds protected LLC-PK1 cells from iodixanol-induced cytotoxicity, oxidative stress, and apoptotic cell death. Pretreatment with compound 8 reversed iodixanol-induced increases in the expression of JNK, ERK, p38, Bax, caspase-3, and caspase-9. It also reversed the iodixanol-induced decrease in Bcl-2 expression. Furthermore, pretreatment with compound 8 caused nuclear translocation of Nrf2 and upregulated HO-1 via the Nrf2 pathway in iodixanol-treated LLC-PK1 cells. Thus, we demonstrated here that compound 8 isolated from A. argyi has the potential to effectively prevent iodixanol-induced kidney epithelial cell death via the caspase- 3/MAPK pathways and HO-1 via the Nrf2 pathway. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
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