Objectives: To explore the possible mechanisms of changes in neural metabolic cells in the white matter injury sites of the brain in mice with carbon monoxide (CO) poisoning and the abnormal absorption of iron ions in the body caused by intestinal flora and intestinal flora disorders.
Methods: C57BL/6 mice were placed in a closed jar and given CO to establish a mouse model of CO poisoning. The control group was given the same treatment but not given CO. Samples were taken from the white matter to observe the morphological changes of white matter, the expression of transferrin (TRF) and glutathione peroxidase 4 (GPX4) was analyzed by immunohistochemistry and Western blotting. Meanwhile, feces of mice were collected at 3rd and 7th day after CO exposure, and 16S rRNA sequencing was performed to analyze the changes of intestinal flora in mice caused by CO poisoning.
Results: Electron microscopy showed that CO poisoning caused obvious demyelination, with increased expression of TRF and decreased expression of GPX4 in the white matter (P<0.05). CO poisoning led to abnormal distribution of intestinal flora in mice, resulting in abnormal absorption of iron in intestinal tissue.
Conclusions: CO poisoning can cause damage to white matter nerve cells in the brain, leading to demyelination. It can also cause abnormal intestinal flora distribution and iron absorption in mice.
目的: 探讨一氧化碳（carbon monoxide，CO）中毒致小鼠脑白质损伤部位神经细胞铁代谢变化及肠道菌群紊乱引起机体铁离子吸收异常的可能机制。方法: 将C57BL/6小鼠置于密闭广口瓶中给予CO气体制作CO中毒小鼠模型，正常对照组予相同处理但不给予CO气体。对小鼠脑白质部位取材，观察脑白质的形态学改变，通过免疫组织化学和蛋白质印迹法分析转铁蛋白（transferrin，TRF）和谷胱甘肽过氧化物酶4（glutathione peroxidase 4，GPX4）的表达变化。同时，于小鼠染毒后3 d和7 d收集粪便，进行16S rRNA测序，分析CO中毒引起的小鼠肠道菌群变化。结果: 电镜结果显示，CO中毒导致小鼠脑白质出现明显脱髓鞘，TRF表达升高（P<0.05），GPX4表达降低（P<0.05）。CO中毒导致小鼠肠道菌群分布异常，致肠组织铁离子吸收异常。结论: CO中毒可导致脑白质神经细胞损伤，进而导致脱髓鞘病变，也可引起小鼠肠道菌群分布和铁离子吸收异常。.
Keywords: carbon monoxide poisoning; demyelination; ferroptosis; forensic pathology; forensic toxicology; intestinal flora; mice; white matter.