Diospyrin modulates inflammation in poly I: C-induced macrophages via ER stress-induced calcium-CHOP pathway
- Authors
- Kim, H.-J.; Khan, I.; Shahidullah, A.; Halimi, S.M.A.; Rauf, A.; Lee, J.-Y.; Kim, Y.-J.; Kim, B.-Y.; Park, W.
- Issue Date
- Sep-2020
- Publisher
- MDPI AG
- Keywords
- Calcium; CHOP; Cytokine; Diospyrin; ER stress; ERK1/2; P38 MAPK; Poly I:C; STAT; Viral infection
- Citation
- Processes, v.8, no.9
- Journal Title
- Processes
- Volume
- 8
- Number
- 9
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/78850
- DOI
- 10.3390/pr8091050
- ISSN
- 2227-9717
- Abstract
- Diospyrin, plant-derived bisnaphthoquinonoid, is known to have anticancer activity. However, pharmacological activity of diospyrin on viral infection is not well known. We investigated effects of diospyrin on macrophages induced by polyinosinic-polycytidylic acid (poly I:C), a mimic of double-stranded viral RNA. Various cytokines, intracellular calcium, nitric oxide (NO), phosphorylated p38 MAPK, and phosphorylated ERK1/2 as well as mRNA expressions of transcription factors were evaluated. Diospyrin significantly reduced NO production, granulocyte-macrophage colony-stimulating factor production, and intracellular calcium release in poly I:C-induced RAW 264.7. The phosphorylation of p38 MAPK and ERK1/2 was also significantly suppressed. Additionally, diospyrin inhibited mRNA levels of nitric oxide synthase 2, C/EBP homologous protein (CHOP), calcium/calmodulin dependent protein kinase II alpha, signal transducers and activators of transcription 1 (STAT1), STAT3, STAT4, Janus kinase 2, first apoptosis signal receptor, c-Jun, and c-Fos in poly I:C-induced RAW 264.7. Taken together, this study represents that diospyrin might have the inhibitory activity against viral inflammation such as excessive production of inflammatory mediators in poly I:C-induced RAW 264.7 via ER stress-induced calcium-CHOP pathway. © 2020 by the authors.
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