Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Aspirin-triggered lipoxin A4 attenuates LPSinduced pro-inflammatory responses by inhibiting activation of NF- B and MAPKs in BV-2 microglial cells | Wang et al. Journal of Neuroinflammation 2011 8 95 http content 8 1 95 JJOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-cB and MAPKs in BV-2 microglial cells 1t 2t 1 2 3 3 1 Yan-Ping Wang Yan Wu Long-Yan Li Jin Zheng Ren-Gang Liu Jie-Ping Zhou Shi-Ying Yuan You Shang1 and Shang-Long Yao1 Abstract Background Microglial activation plays an important role in neurodegenerative diseases through production of nitric oxide NO and several pro-inflammatory cytokines. Lipoxins LXs and aspirin-triggered LXs ATLs are considered to act as braking signals in inflammation. In the present study we investigated the effect of aspirin-triggered LXA4 ATL on inflammatory responses induced by lipopolysaccharide LPS in murine microglial BV-2 cells. Methods BV-2 cells were treated with ATL prior to LPS exposure and the effects of such treatment production of nitric oxide NO inducible nitric oxide synthase iNOS interleukin-1p IL-1Ị3 and tumour necrosis factor-a TNF-a were analysed by Griess reaction ELISA western blotting and quantitative RT-PCR. Moreover we investigated the effects of ATL on LPS-induced nuclear factor-KB NF-kB activation phosphorylation of mitogen-activated protein kinases MAPKs and activator protein-1 AP-1 activation. Results ATL inhibited LPS-induced production of NO IL-1P and TNF-a in a concentration-dependent manner. mRNA expressions for iNOS IL-1P and TNF-a in response to LPS were also decreased by ATL. These effects were inhibited by Boc-2 a LXA4 receptor antagonist . ATL significantly reduced nuclear translocation of NF-kB p65 degradation of the inhibitor WB-a and phosphorylation of extracellular signal-regulated kinase ERK and p38 MAPK in BV-2 cells activated with LPS. Furthermore the DNA binding activity of NF-kB and AP-1 was blocked by ATL. Conclusions This study indicates that ATL inhibits NO and pro-inflammatory cytokine
