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Hong Shan Capsule (HSC) offers radioprotection and modulates acute lethal total-body irradiation-induced alterations of gene expression in rats

ABSTRACT: To further investigate the potential molecular basis of the protective effects of HSC on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays.Pre-treatment with HSC prevented differential expression of 66% (1,398 genes) of 2,126 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 32 pathways, such as olfactory transduction, uroactive ligand-receptor interaction, pathways in cancer, calcium signaling pathway, vascular smooth muscle contraction, cytokine-cytokine receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, peroxisomal proliferator-activated receptor (PPAR）signaling pathway, gonadotropin-releasing hormone (GnRH) signaling pathway, Wnt signaling pathway, janus kinase-signal transducers and activators of transcription (Jak-STAT) signaling pathway, Notch signaling pathway.Our analysis indicated that the pretreatment of rats with HSC attenuated radiation-induced these pathways, such as multiple MAPK pathways, suggesting that the protective effect of HSC acts mainly through the attenuation of these pathways.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE57692 | GEO | 2014/05/15

SECONDARY ACCESSION(S): PRJNA247730

REPOSITORIES: GEO

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Project description:Radiation biodosimetry based on transcriptomic analysis of peripheral blood is a valuable tool to detect radiation exposure after a radiological/nuclear event and obtain useful biological information that could predict tissue and organismal injury. However, confounding factors, including inflammation, can potentially obscure the predictive power of the method. The mitogen-activated protein kinase (MAPK) p38 is normally regulated by the MAP3K-MAP2K pathway in mammalian cells. Members of the p38 MAPK family respond to pro-inflammatory signals and environmental stresses. However, in T cells there is an alternative pathway for p38MAPK activation. This pathway has been shown to play an important role in antigen-receptor-activated T cells and participate in immune and inflammatory responses. Radiation is known to induce a pro-inflammatory response. To examine the role of p38MAPK in response to radiation, we used two mouse models expressing either a p38αMAPK dominant negative (DN) mutation that would be expected to globally suppress p38MAPK signaling or a double knock-in (DKI) mutant, which would be expected to inhibit specifically T cell receptor activation. We exposed wild-type and p38MAPK mutant mice to 7 Gy x-rays and 24 h later we isolated whole blood and performed genome microarray and gene ontology analysis. Comparison between the two mutants (DN, DKI) suggest that the alternative p38MAPK pathway may have wider functions in the response to radiation exposure beyond its well established role as a downstream effector of activated T-cell receptor. Among the differentially enriched pathways, irradiation leads to a significant overrepresentation of pathways associated with morbidity and mortality as well as organismal cell death. In contrast, these pathways were significantly underrepresented in p38MAPKDN and p38MAPKDKI mutant mice, implying that p38MAPK suppression protects mice from the deleterious effects of radiation. Furthermore, radiation exposure resulted in an enrichment of a small number of phagocytosis-related pathways; however, considerably more phagocytosis-related pathways were overrepresented in the p38MAPK mutant mice, implying that p38MAPK signaling, normally, restricts phagocytosis of apoptotic cells after radiation and may, thus, contribute to persistent inflammation. Finally, despite the significant changes in gene expression, we were still able to identify a panel of genes that could accurately distinguish between irradiated and control mice, irrespective of p38MAPK status.

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Hong Shan Capsule (HSC) offers radioprotection and modulates acute lethal total-body irradiation-induced alterations of gene expression in rats

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