Abstract:【Objective】 To explore the effects of X ray irradiation on inflammatory factors expression and biological function in mouse microglia cell line-BV2. 【Methods】 BV2 cells were irradiated by 8 Gy X ray. After irradiation,the expression of inflammatory factors,M1 and M2 cell surface markers were detected with RT-qPCR and flow cytometry. The phagocytic ability of irradiated BV2 cells were evaluated using fluorescein-labeled particles co-culture. The time course changes of MAPKs' (mitogen-activated protein kinase) phosphorylation in irradiated BV2 cells were investigated with Western blotting. Comparison of the proteomic difference between irradiated and unirradiated BV2 cells were performed by mass spectrum identification and bioinformatics analysis. 【Results】 The gene expression of inflammatory factors like IL-1β,TNF-α and the M1 cell surface marker CD86 were significantly upregulated in irradiated cells. Meanwhile,X ray irradiation enhanced BV2 cells' phagocytic ability and increased the phosphorylation level of MAPKs pathway. 【Conclusion】 X ray irradiation drives BV2 cells to M1-like activation and promotes inflammation through the phosphorylation of MAPK pathway.
张海平, 梁栋, 李娓. X射线照射对小鼠小胶质细胞BV2炎症因子表达及细胞生物功能的影响[J]. 医学临床研究, 2023, 40(3): 332-336.
ZHANG Hai-ping, LIANG Dong, LI Wei. Effect of X Ray Irradiation on Inflammatory Factors Expression and Biological Functions in BV2 Cells. JOURNAL OF CLINICAL RESEARCH, 2023, 40(3): 332-336.
[1] LUMNICZKY K,SZATMARI T,SAFRANY G. Ionizing radiation-induced immune and inflammatory reactions in the brain[J].Front Immunol,2017,8:517. [2] MAKALE M T,MCDONALD C R,HATTANGADI-GLUTH J A,et al. Mechanisms of radiotherapy-associated cognitive disability in patients with brain tumours[J].Nat Rev Neurol,2017,13(1):52-64. [3] MONJE M L,MIZUMATSU S,FIKE J R,et al. Irradiation induces neural precursor-cell dysfunction[J].Nat Med,2002,8(9):955-962. [4] MORAVAN M J,OLSCHOWKA J A,WILLIAMS J P,et al.Cranial irradiation leads to acute and persistent neuroinflammation with delayed increases in T-cell infiltration and CD11c expression in C57BL/6 mouse brain[J].Radiat Res,2011,176(4):459-473. [5] FILIANO A J,GADANI S P,KIPNIS J. Interactions of innate and adaptive immunity in brain development and function[J].Brain Res,2015,1617:18-27. [6] MARTINEZ F O,GORDON S. The M1 and M2 paradigm of macrophage activation:time for reassessment[J].F1000Prime Rep,2014,6:13. [7] LIU Y,WU X M,LUO Q Q,et al. CX3CL1/CX3CR1-mediated microglia activation plays a detrimental role in ischemic mice brain via p38MAPK/PKC pathway[J].J Cereb Blood Flow Metab,2015,35(10):1623-1631. [8] HAYASHI Y,FORD L K,FIORITI L,et al. Liquid-Liquid Phase Separation in Physiology and Pathophysiology of the Nervous System[J].J Neurosci,2021,41(5):834-844. [9] ZHOU T,HUANG Z,SUN X,et al. Microglia Polarization with M1/M2 Phenotype Changes in rd1 Mouse Model of Retinal Degeneration[J].Front Neuroanat,2017,11:77. [10] KETTENMANN H. Neuroscience:the brain's garbage men[J].Nature,2007,446(7139):987-989. [11] PEREZ S,RIUS-PEREZ S,TORMOS A M,et al. Age-dependent regulation of antioxidant genes by p38alpha MAPK in the liver[J].Redox Biol,2018,16:276-284. [12] XIN C,QUAN H,KIM J M,et al. Ginsenoside Rb1 increases macrophage phagocytosis through p38 mitogen-activated protein kinase/Akt pathway[J].J Ginseng Res,2019,43(3):394-401. [13] WANG W,WENG J,YU L,et al. Role of TLR4-p38 MAPK-Hsp27 signal pathway in LPS-induced pulmonary epithelial hyperpermeability[J].BMC Pulm Med,2018,18(1):178. [14] MICHEL M C,LI Y,HEUSCH G. Mitogen-activated protein kinases in the heart[J].Naunyn Schmiedebergs Arch Pharmacol,2001,363(3):245-266. [15] BODLES A M,BARGER S W. Secreted beta-amyloid precursor protein activates microglia via JNK and p38-MAPK[J].Neurobiol Aging,2005,26(1):9-16.