急性高浓度PM2.5暴露对小鼠认知能力的影响

流行病学证据表明，老年人长期接触PM2.5可能导致记忆障碍.为了探究短期、严重雾霾天气对人们健康的影响，以C57BL/6J小鼠为研究对象，用不同浓度的PM2.5(0、193、1 930、19 300 μg·kg－1·day－1)，通过鼻腔滴注的实验，染毒1 w，探究急性高浓度PM2.5污染所造成的神经毒性.首先通过Morris水迷宫实验对小鼠认知能力进行检测，暴露结束后对小鼠脑组织进行组织病理学检测(H&E)、氧化应激水平测定(ROS、MDA、SOD).实验结果表明，急性高浓度PM2.5暴露虽然不影响小鼠大脑的生长发育，但会导致小鼠认知能力下降，高剂量19 300 μg·kg－1·day－1PM2.5染毒组小鼠与空白对照组小鼠5 d逃避潜伏期的平均值有显著性差异(为P＜0.05)；小鼠脑组织海马区出现病理学损伤；小鼠脑组织中的ROS水平、MDA含量上升，SOD活性下降.实验揭示了急性高浓度PM2.5暴露对小鼠脑组织能造成氧化损伤，破坏海马神经中枢细胞结构，影响小鼠的学习记忆能力.

Effects of acute high concentration PM2.5 exposure on cognitive ability of mice

Epidemiological evidence suggests that long-term exposure to PM2.5 in the elderly may lead to memory impairment. In order to explore the effects of short-term and severe haze weather on human health， C57BL/6J mice were used to study the neurotoxicity caused by acute high concentration PM2.5 contamination for one week by nasal drip with different concentrations of PM2.5 (0， 193， 1 930， 19 300 μg·kg－1·day－1). In this paper， the cognitive ability of mice exposed to PM2.5 was tested by Morris water maze test， and then the histopathological examination (H&E) and oxidative stress level (ROS， MDA， SOD) were performed in the brain tissue of mice. The results showed that acute exposure to high concentration PM2.5 did not affect the growth and development of mice's brain， but led to a decline in cognitive ability of mice. The average escape latency of mice in high dose PM2.5 exposure group was significantly different from that of mice in blank control group (represents P<0.05). Pathological damage appeared in hippocampus of mice brain tissue， ROS level and MDA content increased， SOD activity decreased in brain tissue of mice. The experiment revealed that acute exposure to high concentration PM2.5 would cause oxidative damage to brain tissue， damage the structure of hippocampal nerve central cells， and affect the learning and memory ability of mice.