Anti-inflammatory effects of tanshinone IIA on radiation-induced microglia BV-2 cells inflammatory response

TY - JOUR

T1 - Anti-inflammatory effects of tanshinone IIA on radiation-induced microglia BV-2 cells inflammatory response

AU - Dong, Xiaorong

AU - Dong, Jihua

AU - Zhang, Ruiguang

AU - Fan, Li

AU - Liu, Li

AU - Wu, Gang

N1 - Keywords: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antibodies, Monoclonal; Cell Survival; Cells, Cultured; DNA Primers; Inflammation; Mice; Microglia; Phenanthrenes; Polymerase Chain Reaction; RNA; Radiotherapy

PY - 2009

Y1 - 2009

N2 - AIM: The aim of this study was to explore the inhibitory effects of Tanshinone II(A) 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 microg/mL of Tanshinone II(A). The effects of Tanshinone II(A) on radiation-induced proinflammatory cytokines were evaluated by real-time polymerase chain reaction; the expression level of nuclear factor (NF-kappabeta) 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 II(A) decreased the radiation-induced release of proinflammatory cytokines. Further, Western blotting showed that Tanshinone II(A) could attenuate the nuclear translocation of (NF-kappabeta) p65 submit postirradiation. Immunofluorescence staining showed gamma-H2AX foci formation with p65 translocation into the nucleus postirradiation. CONCLUSIONS: Our data indicated that Tanshinone II(A) exerts anti-inflammatory properties by suppressing the transcription of proinflammatory cytokine genes that might be associated with the NF-kappabeta signaling pathway. It is postulated that irradiation causes immediate cellular reaction, and that double-strand breaks trigger the molecular response that leads to NF-kappabeta pathway activation.

AB - AIM: The aim of this study was to explore the inhibitory effects of Tanshinone II(A) 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 microg/mL of Tanshinone II(A). The effects of Tanshinone II(A) on radiation-induced proinflammatory cytokines were evaluated by real-time polymerase chain reaction; the expression level of nuclear factor (NF-kappabeta) 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 II(A) decreased the radiation-induced release of proinflammatory cytokines. Further, Western blotting showed that Tanshinone II(A) could attenuate the nuclear translocation of (NF-kappabeta) p65 submit postirradiation. Immunofluorescence staining showed gamma-H2AX foci formation with p65 translocation into the nucleus postirradiation. CONCLUSIONS: Our data indicated that Tanshinone II(A) exerts anti-inflammatory properties by suppressing the transcription of proinflammatory cytokine genes that might be associated with the NF-kappabeta signaling pathway. It is postulated that irradiation causes immediate cellular reaction, and that double-strand breaks trigger the molecular response that leads to NF-kappabeta pathway activation.

U2 - 10.1089/cbr.2009.0640

DO - 10.1089/cbr.2009.0640

M3 - Journal article

C2 - 20025548

SN - 1084-9785

VL - 24

SP - 681

EP - 687

JO - Cancer Biotherapy & Radiopharmaceuticals

JF - Cancer Biotherapy & Radiopharmaceuticals

IS - 6

ER -