Illumina microarray analysis of brain regions following acute exposure to bilirubin or LPS

We developed a novel mouse model of acute bilirubin toxicity. 450mg/kg bilirubin was administered IP to mice, which exhibited transient hearing deficits and ataxia at 4 hours, and recovered by 24 hours. This toxicity is consistent with the human symptoms of bilirubin toxicity. To investigate the molecular mechanisms of bilirubin toxicity we carried out whole genome gene expression analysis on gross brain regions (cortex, cerebellum and brainstem) and specific parts of the auditory pathway (MNTB and CN) at 2 hours, 4 hours and 24 hours post injection. We detected several transcriptional markers of neuroinflammation, and so developed a second set of data for the same brain regions and time points following injection of a well characterized neuroinflammatory agent; LPS (5mg/kg).我们开发了一种新型急性胆红素毒性小鼠模型。以450mg/kg的剂量对小鼠实施腹腔注射（intraperitoneal, IP）胆红素，小鼠于注射后4小时出现一过性听力损伤与共济失调，并于24小时恢复。该毒性表型与人类胆红素毒性的临床症状一致。为探究胆红素毒性的分子机制，我们在注射后2小时、4小时及24小时，对大体脑区（大脑皮层、小脑及脑干）以及听觉通路的特定核团——斜方体内侧核（medial nucleus of the trapezoid body, MNTB）与蜗核（cochlear nucleus, CN）开展了全基因组基因表达分析。本研究检测到多种神经炎症相关转录标志物，因此针对相同脑区与时间节点，在注射经充分表征的神经炎症诱导剂脂多糖（lipopolysaccharide, LPS，5mg/kg）后，额外采集了第二组数据集。