The favorable responses of crop species to low-dose γ irradiation can help to develop cultivars with increased productivity and improved stress tolerance. In the present study, we tried to reveal the candidate metabolites involved in growth stimulation of barley seedlings after applying low-dose γ-radiation (60Co) to seeds. Stimulating doses (5-20 Gy) provided a significant increase in shoot length and biomass, while relatively high dose of 100 Gy led to significant inhibition of growth. Gas chromatography-mass spectrometry metabolomic analysis uncovered several compounds that may take part in radiation hormesis establishment in irradiated plants. This includes molecules involved in nitrogen redistribution (arginine, glutamine, asparagine, and γ-aminobutyric acid) and stress-responsive metabolites, such as ascorbate, myo-inositol and its derivates, and free amino acids (l-serine, β-alanine, pipecolate, and GABA). These results contribute to the understanding of the molecular mechanisms of hormesis phenomenon. © The Author(s) 2020.Exposure to ionizing radiation is a major threat to human health and public security. Since the inherent limitations of current methods for indicating radiation exposure, new minimally invasive biomarkers that can be easily and quickly detected at an early stage are needed for optimal medical treatment. Serum proteins are attractive biomarkers and some radiosensitive proteins have been found, but the proteins in response to low-dose and high-linear energy transfer (LET) radiation have not been reported. In this study, mice were whole body exposed to a variety doses of carbon ions and X-rays. We performed Mouse Antibody Array to detect serum proteins expression profiles at 24 hours postirradiation. After conditional screening, insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-1 (IGFBP-1), and IGFBP-3 were further validated using enzyme-linked immunosorbent assay. After exposure to 0.05 to 1 Gy of carbon ions and 0.5 to 4 Gy of X-rays, only IGFBP-3 showed obvious increase with increased doses, both carbon ions and X-rays. Further, IGFBP-3 was detected for observation of its time-dependent changes. The results showed the expression difference of IGFBP-3 presented from 6 to 24 hours post-irradiation by carbon ions and X-rays. Moreover, the receiver-operating characteristic analysis showed that serum IGFBP-3 is efficient to triage exposed individuals with high sensitivity and specificity. These results suggest that serum IGFBP-3 is extremely sensitive to high- and low-LET ionizing radiation and is able to respond at an early stage, which could serve as a novel minimally invasive indicator for radiation exposure. © The Author(s) 2020.Adenosine deaminase acting on double-stranded RNA 1 (ADAR1) mediates adenosine-to-inosine (A-to-I) RNA editing events.  https://www.selleckchem.com/products/GDC-0980-RG7422.html  ADAR1 is highly expressed in "septic" macrophages and in small intestinal tissues of mice with sepsis. Overexpression of ADAR1 suppresses inflammation and intestinal damage. However, the specific underlying mechanism is unclear. This study was conducted to explore how microRNA (miRNA) regulates the anti-inflammatory mechanism of macrophages following ADAR1 upregulation. A murine sepsis model was established by cecal ligation and puncture (CLP). Mice were randomly assigned to sham, CLP, and CLP+ADAR1 groups. Hematoxylin and eosin (HE) staining and fluorescence isothiocyanate-dextran were used to evaluate intestinal injury and permeability. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blotting, and Luminex assays were performed to detect changes in the expression of inflammatory cytokines. Adenoviruses were used to express ADAR1 in RAW 264.7 cells. Ribonucleoprotein immunoprecipitation analysis was conducted to detect the binding of ADAR1 and miRNAs. A dual-luciferase reporter assay was used to detect the binding of miRNAs and regulatory factors. We observed that ADAR1 significantly increased the expression of suppressor of cytokine signaling 3 (SOCS3) in macrophages and reduced the expression of interleukin-6 in macrophages and the serum, thereby reducing intestinal permeability and mucosal injury in mice with sepsis. The RNA-ribonucleoprotein immunoprecipitation binding assay and qRT-PCR demonstrated a direct interaction between ADAR1 and pri-miR-30a. The luciferase assay demonstrated that SOCS3 was significantly inhibited by miR-30a-5p, the mature product of miR-30a. Thus, ADAR1 exerts a protective effect against sepsis by reducing inflammation and organ damage via the ADAR1-miR-30a-SOCS3 axis. Copyright © 2020 Zhou Shangxun et al.Neuropathic pain is a serious clinical problem to be solved. This study is aimed at investigating protein kinase A (PKA) expression in neuropathic pain and its possible mechanisms of involvement. A neuropathic pain-related gene expression dataset was downloaded from Gene Expression Omnibus, and differentially expressed genes were screened using the R software. cytoHubba was used to screen for hub genes. A spared nerve injury (SNI) rat model was established, and the paw withdrawal threshold was determined using von Frey filaments. Western blotting and immunofluorescence were used to detect the expression and cellular localization, respectively, of key proteins in the spinal cord. Western blot, ELISA, and TUNEL assays were used to detect cell signal transduction, inflammation, and apoptosis, respectively. Pka was identified as a key gene involved in neuropathic pain. After SNI, mechanical allodynia occurred, PKA expression in the spinal cord increased, the p38MAPK pathway was activated, and spinal cord inflammation and apoptosis occurred in rats. PKA colocalized with neurons, astrocytes, and microglia, and apoptotic cells were mainly neurons. Intrathecal injection of a PKA inhibitor not only relieved mechanical hyperalgesia, inflammatory reaction, and apoptosis in SNI rats but also inhibited p38MAPK pathway activation. However, intrathecal injection of a p38MAPK inhibitor attenuated mechanical hyperalgesia, inflammation, and apoptosis, but did not affect PKA expression. In conclusion, PKA is involved in neuropathic pain by activating the p38MAPK pathway to mediate spinal cord cell apoptosis. Copyright © 2020 Yajun Deng et al.