RESUMO
Low-temperature plasma (LTP) is an emerging biomedical technique that has been proposed as a potential approach for cancer therapy. Meanwhile, berberine (BER), an active ingredient extracted from various medical herbs, such as Coptischinesis, has been proven antitumor effects in a broad spectrum of cancer cells. In this study, we seek to develop a novel dual cancer therapeutic method by integrating pre-administration of BER and LTP exposure and evaluating its comprehensive antitumor effect on the human non-small-cell lung cancer (NSCLC) cell lines (A549 and H1299) in vitro. Cell viability, cell cycle, cell apoptosis, and intracellular and extracellular ROS were investigated. The results showed that cotreatment of BER and LTP significantly decreased the cell viability, arrested the cell cycle in the S phase, promoted cell apoptosis, and increased intracellular and extracellular ROS. Additionally, RNA Sequencing (RNA-Seq) technology was used to explore potential mechanisms. The differentially expressed genes among different treatment groups of NSCLC cells were analyzed and were mainly enriched in the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Moreover, cotreatment of BER and LTP notably depressed the total protein expression level of PI3K and AKT with immunoblotting. In conclusion, BER and LTP have a synergistic inhibitory effect on NSCLC cells via the PI3K-AKT signaling pathway, which could provide a promising strategy for supplementary therapy in the anti-NSCLC battle.
Assuntos
Berberina , Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Humanos , Carcinoma Pulmonar de Células não Pequenas/patologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Berberina/farmacologia , Berberina/uso terapêutico , Neoplasias Pulmonares/patologia , Fosfatidilinositol 3-Quinase/metabolismo , Espécies Reativas de Oxigênio/farmacologia , Temperatura , Linhagem Celular Tumoral , Proliferação de Células , Transdução de Sinais , ApoptoseRESUMO
KylinRay-IMRT is the advanced radiotherapy treatment planning module of accurate radiotherapy system (KylinRay) aiming to provide accurate and efficient plan design platform. In this paper the system design, main functions and key technologies of KylinRay-IMRT were introduced. KylinRay-IMRT supports three dimensional conformal radiotherapy (3D-CRT), intensity modulated radiotherapy (IMRT) and many other types of treatment plan design with function modules including patient data management, image registration and fusion, image contouring, image three dimensional reconstruction and visualization, three dimensional conformal radiotherapy planning, intensity modulated radiotherapy planning, plan evaluation and comparison, and report print. KylinRay-IMRT has been tested by the national standard YY/T 0889-2013, the results showed that the performance of KylinRay-IMRT can fully meet the standard requirements.
Assuntos
Planejamento da Radioterapia Assistida por Computador , Radioterapia de Intensidade Modulada , Humanos , Dosagem Radioterapêutica , Radioterapia Conformacional , Tomografia Computadorizada por Raios XRESUMO
Utilizing the energy released from the nuclear fusion of deuterium with tritium (DT) may be an important method of supplying energy in the future. The ionizing radiation emitted from nuclear fusion is a potential health risk to humans, including scientists who are currently performing nuclear fusion experiments and the employees of fusion nuclear plants, in the future. However, there have been few reports on the biological effects of fusion radiation. In the present study, using the High Intensity DT Fusion Neutron Generator, the DNA damage and its regulation in normal human fibroblasts exposed to fusion radiation were investigated. Heme oxygenase 1 (HO1), which is reported to induce antiinflammatory activity, was upregulated in the irradiated cells. Pretreatment with the HO1 inhibitor, protoporphyrin IX zinc (II), exacerbated double strand break formation following exposure to fusion radiation. The expression of cyclooxygenase2 (COX2) contributed to the upregulation of HO1, as demonstrated by the result that its inhibitor, NS398, inhibited the induction of HO1 in irradiated cells. It was further clarified that the ataxia telangiectasia mutated DNA damage response was activated and it stimulated the phosphorylation of p38 mitogenactivated protein kinase, which was responsible for the upregulation of COX2 and HO1. These results provide novel information on fusion radiationinduced biological effects and potential targets for decreasing the associated health risks.