期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 265, 期 1-2, 页码 36-42出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2013.09.014
关键词
Interleukin-13; Interleukin-4; Prothrombin kringle-2; Microglia; NADPH oxidase; COX-2
资金
- National Research Foundation of Korea (NRF)
- Korean Government (MSIP) [2008-0061888]
The present study examined whether Interleukin-13 (IL-13) or IL-4, an anti-inflammatory cytokine, could induce cell death of activated microglia by prothrombin kringle-2 (pKr-2) which is a domain of prothrombin distinct from thrombin. Microglia cell death was detected at eight days after co-treatment of pKr-2 with IL-13/IL-4 in vitro. This cell death was assessed by live assay, dead assay, TUNEL and MU assay. In parallel, reactive oxygen species (ROB) production was evident as assessed by superoxide assay, WST-1 and analyzing DCF in combination of pKr-2 and IL-13 or IL-4 treated microglia. The IL-13/IL-4-enhanced ROS production and cell death in pKr-2 activated microglia was partially inhibited by an NADPH oxidase inhibitor, apocynin and/or by several antioxidants. Moreover, Western blot analysis showed a significant increase in cyclooxygenase-2 (COX-2) expression in combination of pKr-2 and IL-13 or IL-4 treated microglia, which was partially inhibited by apocynin and an antioxidant, trolox. Additional studies demonstrated that microglia cell death was reversed by treatment with COX-2 inhibitor, NS398. Our data strongly suggest that oxidative stress and COX-2 activation through NADPH oxidase may contribute to IL-13/IL-4 induced cell death of pKr-2 activated microglia. (C) 2013 Elsevier B.V. All rights reserved.
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