期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 385, 期 2, 页码 132-136出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.04.041
关键词
HMGB1; Minocycline; PC12; OGD; p38MAPK; ERK1/2
资金
- Ministry of Education, culture. Sports, Science, and Technology of Japan [17100007, 21390483]
- Health and Labor Sciences Research Grant from the Ministry of Health, Labor and Welfare
- Grants-in-Aid for Scientific Research [17100007, 21390483] Funding Source: KAKEN
High mobility group box-1 (HMGB1), a non-histone DNA-binding protein, is massively released into the extracellular space from neuronal cells after ischemic insult and exacerbates brain tissue damage in rats. Minocycline is a semisynthetic second -generation tetracycline antibiotic which has recently been shown to be a promising neuroprotective agent. In this Study, we found that minocycline inhibited HMGB1 release in oxygen-glucose deprivation (OGD)-treated PC12 cells and triggered the activation of p38mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK1/2). The ERK kinase (MEK)1/2 inhibitor U-0126 and p38MAPK inhibitor SB203580 blocked HMGB1 release in response to OGD. Furthermore, HMGB1 triggered cell death in a dose-dependent fashion. Minocycline significantly rescued HMGSB1-induced cell death in a close-dependent manner. In light of recent observations as well as the good safety profile of minocycline in humans. we propose that minocycline might play a potent neuroprotective role through the inhibition of HMGB1-induced neuronal cell death in cerebral infarction. (C) 2009 Elsevier Inc. All rights reserved.
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