Cikla Ulas, Chanana Vishal, Kintner Douglas B, Covert Lucia, Dewall Taylor, Waldman Alex, Rowley Paul, Cengiz Pelin, Ferrazzano Peter
Waisman Center, University of Wisconsin, Madison, WI 53705, USA.
Waisman Center, University of Wisconsin, Madison, WI 53705, USA; Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA.
J Neuroimmunol. 2016 Feb 15;291:18-27. doi: 10.1016/j.jneuroim.2015.12.004. Epub 2015 Dec 12.
We previously found increased microglial proliferation and pro-inflammatory cytokine release in infant mice compared to juvenile mice after hypoxia-ischemia (HI). The aim of the current study was to assess for differences in the effect of microglial suppression on HI-induced brain injury in infant and juvenile mice. HI was induced in neonatal (P9) and juvenile (P30) mice and minocycline or vehicle was administered at 2h and 24h post-HI. P9 minocycline-treated mice demonstrated early but transient improvements in neurologic injury, while P30 minocycline-treated mice demonstrated sustained improvements in cerebral atrophy and Morris Water Maze performance at 60days post-HI.
我们之前发现，与幼鼠相比，缺氧缺血（HI）后幼龄小鼠的小胶质细胞增殖增加且促炎细胞因子释放增多。本研究的目的是评估抑制小胶质细胞对幼龄和成年小鼠HI诱导的脑损伤影响的差异。在新生（P9）和成年（P30）小鼠中诱导HI，并在HI后2小时和24小时给予米诺环素或赋形剂。P9米诺环素治疗的小鼠在神经损伤方面表现出早期但短暂的改善，而P30米诺环素治疗的小鼠在HI后60天时脑萎缩和莫里斯水迷宫表现方面持续改善。
