PM_2.5 exposure is an emerging environmental concern and severe health insult closely related to psychological conditions such as anxiety and depression in adolescence. Adolescence is a critical period for neural system development characterized by continuous brain maturation, especially in the prefrontal cortex. The etiology of these adolescent conditions may derive from fetal origin, probably attributed to the adverse effects induced by intrauterine environmental exposure. Anxiety- and depression-like behavior can be induced by gestational exposure to PM_2.5 in mice offspring which act as a useful model system. Recent studies show that B-vitamin may alleviate PM_2.5-induced hippocampal neuroinflammation- and function-related spatial memory impairment in adolescent mice offspring. However, cortical damage and related neurobehavioral defects induced by gestational PM_2.5 exposure, as well as the potential reversibility by interventions in mice offspring require to be elucidated. Here, we aimed to investigate whether B-vitamin would protect mice offspring from the adverse effects derived from gestational exposure to urban PM_2.5 on cortical areas to which anxiety and depression are closely related. Pregnant mice were divided into three groups: control group (treated with PBS alone), model group (treated with both PM_2.5 and PBS), and intervention group (treated with both PM_2.5 and B-vitamin), respectively. The mice offspring were then applied to comprehensive neurobehavioral, ultrastructural, biochemical, and molecular biological analyses. Interestingly, we observed that gestational PM_2.5 exposure led to neurobehavioral defects including anxiety- and depression-like behavior. In addition, neuroinflammation, oxidative damage, increased apoptosis, and caspase-1-mediated inflammasome activation in the prefrontal cortex were observed. Notably, both behavioral and molecular changes could be significantly alleviated by B-vitamin treatment. In summary, our results suggest that the anxiety- and depression-like behavior induced by gestational PM_2.5 exposure in mice offspring can be ameliorated by B-vitamin supplementation, probably through the suppression of apoptosis, oxidative damage, neuroinflammation, and caspase-1-mediated inflammasome activation.

PM _2.5暴露是一种新出现的环境问题，严重的健康侮辱与心理状况（如青春期的焦虑和抑郁）密切相关。青春期是神经系统发育的关键时期，其特征是持续的大脑成熟，尤其是在额叶前皮质。这些青春期疾病的病因可能来自胎儿，可能归因于宫内环境暴露引起的不良影响。可以通过妊娠暴露于小鼠后代的PM _2.5来诱发焦虑和抑郁样行为，这是一种有用的模型系统。最近的研究表明，维生素B可以缓解PM _2.5引起的青春期小鼠后代海马神经炎症和功能相关的空间记忆障碍。但是，需要阐明由于妊娠PM _2.5暴露引起的皮层损害和相关的神经行为缺陷，以及通过干预小鼠后代的潜在可逆性。在这里，我们旨在研究B-维生素是否能保护小鼠后代免受妊娠与城市PM _2.5的妊娠接触对与焦虑和抑郁密切相关的皮质区域的不利影响。将怀孕的小鼠分为三组：对照组（仅用PBS处理），模型组（用PM _2.5和PBS处理）和干预组（同时用PM _2.5处理）和B-维生素）。然后将小鼠后代应用于综合的神经行为，超微结构，生化和分子生物学分析。有趣的是，我们观察到妊娠PM _2.5暴露会导致神经行为缺陷，包括焦虑和抑郁样行为。此外，观察到前额叶皮层中的神经炎症，氧化损伤，凋亡增加和胱天蛋白酶-1介导的炎性体活化。值得注意的是，行为和分子变化均可通过B-维生素治疗得到显着缓解。总而言之，我们的研究结果表明妊娠PM _2.5诱发的焦虑和抑郁样行为 补充维生素B可以改善小鼠后代的暴露，可能是通过抑制细胞凋亡，氧化损伤，神经炎症和caspase-1介导的炎症小体活化来实现的。