Xu Ranhong, Chen Haiyu, Wang Yougang, Qi Haomin, Chen Yinuo, Dai Anqi, Yang Siqi, Wang Yue, Zeng Yan, Li Jinquan
Hubei Clinical Research Center for Alzheimer's Disease, Brain Science and Advanced Technology Institute, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Hubei Clinical Research Center for Alzheimer's Disease, Brain Science and Advanced Technology Institute, School of Medicine, Wuhan University of Science and Technology, Wuhan, China; Geriatric Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, Hubei Province, China.
J Hazard Mater. 2025 Mar 5;485:136901. doi: 10.1016/j.jhazmat.2024.136901. Epub 2024 Dec 17.
In recent years, there has been a notable increase in the concentration of air pollutants in the troposphere, especially ozone. However, limited research has gone beyond examining histopathological alterations in the olfactory bulb (OB) to explore the effects of ozone exposure on olfactory and cognitive functions. In our study, we exposed nine-month-old C57BL/6 mice to ozone at a concentration of 1.0 ppm for 13 weeks to examine the effects of ozone on the OB. The results indicated that ozone exposure induces olfactory and cognitive impairments in the mice. Subsequently, microglia in the OB are activated, leading to neuroinflammation. Ozone-induced downregulation of PSD95 and Synaptophysin, which was accompanied by a decrease in dendritic length and spine density. Simultaneously, increasing in the co-labeling of C1q, Iba1, and PSD95 after ozone exposure indicated that C1q-mediated synaptic phagocytosis by microglia might play a role in synaptic damage. Furthermore, the co-labeling of GSDMD-N and NEUN results suggests that ozone exposure triggers pyroptosis in neurons. Additionally, minocycline administration can alleviate ozone-induced olfactory and cognitive impairments by suppressing microglial activation. This study illustrates that prolonged ozone exposure leads to microglial activation in the OB, causing synaptic damage, neuronal pyroptosis, and subsequent deficits in olfactory and cognitive functions.
近年来，对流层中空气污染物的浓度显著增加，尤其是臭氧。然而，有限的研究仅停留在检查嗅球（OB）的组织病理学改变，而未深入探讨臭氧暴露对嗅觉和认知功能的影响。在我们的研究中，我们将9个月大的C57BL/6小鼠暴露于浓度为1.0 ppm的臭氧环境中13周，以研究臭氧对嗅球的影响。结果表明，臭氧暴露会导致小鼠出现嗅觉和认知障碍。随后，嗅球中的小胶质细胞被激活，引发神经炎症。臭氧导致PSD95和突触素下调，同时伴有树突长度和棘密度的降低。同时，臭氧暴露后C1q、Iba1和PSD95的共标记增加，表明小胶质细胞介导的C1q突触吞噬可能在突触损伤中起作用。此外，GSDMD-N和NEUN的共标记结果表明，臭氧暴露会触发神经元焦亡。此外，给予米诺环素可通过抑制小胶质细胞激活来减轻臭氧诱导的嗅觉和认知障碍。这项研究表明，长期臭氧暴露会导致嗅球中的小胶质细胞激活，引起突触损伤、神经元焦亡，进而导致嗅觉和认知功能缺陷。
