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Purpose: Blast lung injury (BLI) is the most common damage resulted from explosion-derived shock wave in military, terrorism and industrial accidents. However, the molecular mechanisms underlying BLI induced by shock wave are still unclear. Methods: In this study, a goat BLI model was established by a fuel air explosive power. The key genes involved in were identified. The goats of the experimental group were fixed on the edge of the explosion cloud, while the goats of the control group were 3 km far away from the explosive environment. After successful modeling for 24 h, all the goats were sacrificed and the lung tissue was harvested for histopathological observation and RNA sequencing. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analysis were performed to identify the main enriched biological functions of differentially expressed genes (DEGs). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to verify the consistency of gene expression. Results: Of the sampled goat lungs, 895 genes were identified to be significantly differentially expressed, and they were involved in 52 significantly enriched GO categories. KEGG analysis revealed that DEGs were highly enriched in 26 pathways, such as cytokine-cytokine receptor interaction, antifolate resistance, arachidonic acid metabolism, amoebiasis and bile secretion, JAK-STAT, and IL-17 signaling pathway. Furthermore, 15 key DEGs involved in the biological processes of BLI were confirmed by qRT-PCR, and the results were consistent with RNA sequencing. Conclusion: Gene expression profiling provide a better understanding of the molecular mechanisms of BLI, which will help to set strategy for treating lung injury and preventing secondary lung injury induced by shock wave.

The potential antitumor application of low-temperature plasma (LTP) has attracted wide attention from researchers. The mechanism of plasma antitumor action may be related to LTP-induced reactive oxygen and nitrogen species. The aim of this study was to identify the apoptotic effects of plasma on melanoma cells (B16) in vivo and in vitro. For this purpose, a helium atmospheric-pressure plasma jet (APPJ) was used to generate the plasma-activated saline and medium (PAS and PAM). The PAS was injected subcutaneously to treat B16-tumor bearing mice in vivo and the PAM was used to treat B16 cells in vitro. Catalase (CAT) was added into the PAM to degrade H2O2 as the intervention group. The tumor nodules’ weight, cryosections, B16 cell viability, apoptosis, DNA damage, p53 pathway-related protein and the concentration of H2O2 in PAM were detected. The in vivo results showed that PAS could inhibit tumor growth and induce apoptosis. The in vitro results revealed the concentration of H2O2 in the PAM increased as LTP treatment time was longer, while the cell viability decreased as APPJ irradiation time was increased. Flow cytometry results showed that, compared with the control group, all PAM treatment groups showed a higher apoptotic rate. A single cell gel assay and an 8-OHdG assay showed that the PAM could induce DNA damage. A western blotting assay indicated that the PAM could increase the expressions of p53, p53-induced gene 8 protein, PIG3, cytoplasmic cytochrome c, cleaved-caspase-9 and -3. However, CAT could alleviate all these changes effectively. These findings suggested that plasma exerted an apoptotic effect on B16 cells mainly by activating the p53/PIGs/caspase pathway. [ABSTRACT FROM AUTHOR]