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- Title
Transcriptome profiling of poly(I:C)-induced RAW 264.7 mouse macrophages in response to panaxadiol.
- Authors
Yang, Zhou-Xin; Guo, Dong-Yang; Shen, Ling-Zhi; Mao, Gen-Xiang; Dai, Ji-Huan; Chen, Sha-Sha; Yan, Jing
- Abstract
Panaxadiol is an active compound in steamed ginseng that possesses anti-cancer properties. Nonetheless, the effect of panaxadiol on inflammation remains unclear. Double-stranded RNA (dsRNA) acts as a molecular mimic associated with viral infection. It is recognized by Toll-like receptor-3 (TLR3), and it induces pro-inflammatory cytokines production of immune cells-like macrophages. Synthetic dsRNA polyriboinosinic polyribocytidylic acid [Poly(I:C)] is structurally similar to double-stranded RNA, which is used to simulate dsRNA in inducing immune response. In this study, we used an RNA-Seq based approach to analyze changes in mRNA level of poly (I:C)-induced RAW264.7 treated by panaxadiol. First, our data suggested that 20 μM and 40 μM panaxadiol may reduce poly(I:C)-induced RAW264.7 cell viability, while the concertation of 10 μM panaxadiol was enough to inhibit the cell production of TNF-α and IL-6. Next, 10 μM panaxadiol was applied to investigate the transcriptome profile change of Poly(I:C)-induced RAW264.7 cells. Transcriptome profile showed that inflammatory related genes (such as Cxcl2, Csf3, Ptgs2, Acod1, Lif and Il1b) could be downregulated by panaxadiol, which was confirmed by real-time PCR. Moreover, Gene Ontology enrichment analysis showed that downregulated genes were associated with immune responses, while many upregulated genes were related to DNA replication. In addition, KEGG enrichment showed changes of pathways like NF-kappa B signaling pathway and DNA replication after treatment with panaxadiol. To sum up, our results suggested that panaxadiol may inhibit inflammatory associated genes in macrophages induced by poly(I:C). Considering its anti-virus effects, panaxadiol could be used to treat a variety of virus related diseases.
- Subjects
DOUBLE-stranded RNA; DNA replication; CELL survival; VIRUS diseases; IMMUNE response; GENE ontology; MACROPHAGES
- Publication
Biologia, 2019, Vol 74, Issue 10, p1385
- ISSN
0006-3088
- Publication type
Article
- DOI
10.2478/s11756-019-00288-x