Your conditions: Radiobiology
  • Protective Effect of IGFBP-3 Protein on Heavy Ion Radiation Induced Injury in Mice

    Subjects: Physics >> Nuclear Physics Subjects: Biology >> Radiobiology submitted time 2024-05-06

    Abstract: Manned spaceflight and nuclear technology applications are running on a highway in China today. The radiation and nuclear safety will continue to be a major national demand in a long term. Thus, the continuous observation of new radiation protection molecular targets and related drugs is of great value to us. Our previous study has found that the circulating Insulin-like Growth Factor Binding Protein 3 (IGFBP-3) showed a significant increase after total body exposure of mice to ionizing radiation. However, the function of IGFBP-3 and the effects of it level change on radiation induced damages are still unclear. In this study, we set up the Igfbp3 gene overexpression and knock-down cell models in mouse Kupffer (MKC) cells. The CCK-8 assay, EdU assay, clone formation assay and microsphere phagocytosis experiment were performed for investing the proliferation activity, DNA replication activity and phagocytic ability of different cell models after carbon-ion irradiation. Moreover,mice were tail vein injected with recombinant IGFBP-3 protein at 2 hours before 5 Gy carbon-ion irradiation, and the survival curves of mice were drawn. The results showed that overexpression of IGFBP-3 protein significantly alleviated the radiation-induced decrease of the DNA replication activity, cell viability, clone formation rate, and phagocytic ability of MKC cells. On the contrary, the knock-down of IGFBP-3 protein expression reduced the above results. Injection of IGFBP-3 protein before carbon-ion exposure significantly delayed the time of death in mice. Our results indicate at the cellular and animal levels that IGFBP-3 protein has the potential to reduce radiation-induced damages and serve as a target for radiation protection. Through enhancing the radiation resistance and phagocytic ability of Kupffer cells in mice to reduce the risk of infection after radiation exposure might be the underlying mechanism of the effects of IGFBP-3 on radiation protection.

  • Mitochondrial ribosomal protein MRPS28 participates in apoptosis of A549 cells induced by carbon ion irradiation

    Subjects: Biology >> Radiobiology submitted time 2023-08-08

    Abstract: Purpose: To investigate the mechanism by which mitochondrial ribosomal protein MRPS28 affects carbon ion irradiation-induced apoptosis in A549 cells.
    Methods: siRNA was used to knock down MRPS28 and establish a stable MRPS28-knockdown A549 cell line; Cells were irradiated with carbon ion and X-ray; CCK-8 assay was performed to assess cell proliferation; Clonogenic survival assay measured cell survival rate; Flow cytometry detected apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential; qRT-PCR examined relevant genes; Western Blot analyzed apoptosis-related proteins.
    Results: Exposure of non-small cell lung cancer A549 cells to carbon ion irradiation led to decreased MRPS28 expression; Compared to the control group, MRPS28 knockdown reduced A549 cell proliferation and clonogenic survival, increased ROS levels, decreased mitochondrial membrane potential, and induced apoptosis through the p53-mediated mitochondrial apoptotic pathway; MRPS28 knockdown combined with carbon ion irradiation significantly reduced A549 cell proliferation and survival, promoting apoptosis after irradiation.
    Limitation: MRPS28 down-regulation increased the sensitivity of A549 cells to carbon ion irradiation, but the specific mechanism requires further investigation.
    Conclusion: This study preliminarily demonstrates that MRPS28 down-regulation is involved in carbon ion irradiation-induced apoptosis in A549 cells and enhances A549 cell sensitivity to carbon ion.

  • Study on the mechanism for Danggui anti-carbon ion radiation based on network pharmacology

    Subjects: Biology >> Radiobiology submitted time 2023-07-19

    Abstract: [Objective] Network pharmacology technology was used to explore the mechanism of Danggui anti-carbon radiation.
    [Methods] Danggui active ingredients and Targets of Danggui anti-carbon ion radiation were obtained through related databases. Target biological networks were constructed, bioinformatics analysis of targets were conducted. Molecular docking was performed to verify the results of network pharmacology.
    [Results] Nine active ingredients of Danggui participate in signaling pathways such as PI3K-AKT and MAPK through ninety-eight targets, regulate molecular functions such as DNA binding, kinase binding, and DNA damage response and other processes. Molecular docking verifies the reliability of network pharmacological results.
    [Limitations] The results of network pharmacology were only verified by molecular docking.