Anti-Inflammatory Effects of Tanshinone IIA on Radiation-Induced Microglia BV-2 Cells Inflammatory Response

作者：Dong Xiaorong; Dong Jihua; Zhang Ruiguang; Fan Li; Liu Li; Wu Gang^*

来源：Cancer Biotherapy and Radiopharmaceuticals, 2009, 24(6): 681-687.

DOI：10.1089/cbr.2009.0640

• irradiation
• DNA double-strand break
• microglia cells inflammatory response
• Tanshinone IIA

Aim: The aim of this study was to explore the inhibitory effects of Tanshinone IIA on the production of proinflammation cytokines in radiation-stimulated microglia.
Methods: Microglia cells were treated with 2, 4, 8, 16, and 32 Gy of irradiation or sham-irradiated in the presence or absence of 1.0 mu g/mL of Tanshinone IIA. The effects of Tanshinone IIA on radiation-induced proinflammatory cytokines were evaluated by real-time polymerase chain reaction; the expression level of nuclear factor (NF-kappa beta) p65 in cytoplasm and nucleus was measured by Western blot. Immunofluorescence staining and confocal microscopy analysis were applied to detect the expression of gamma-H2AX and p65 postirradiation.
Results: Radiation-induced release of proinflammatory cytokines in BV-2 cells was detectable after irradiation. Tanshinone IIA decreased the radiation-induced release of proinflammatory cytokines. Further, Western blotting showed that Tanshinone IIA could attenuate the nuclear translocation of (NF-kappa beta) p65 submit postirradiation. Immunofluorescence staining showed gamma-H2AX foci formation with p65 translocation into the nucleus postirradiation.
Conclusions: Our data indicated that Tanshinone IIA exerts anti-inflammatory properties by suppressing the transcription of proinflammatory cytokine genes that might be associated with the NF-kappa beta signaling pathway. It is postulated that irradiation causes immediate cellular reaction, and that double-strand breaks trigger the molecular response that leads to NF-kappa beta pathway activation.

• 出版日期2009-12
• 单位华中科技大学