Neuropathology changed by 3- and 6-months low-level PM 2.5 inhalation exposure in spontaneously hypertensive rats
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(2020) 17:59
RESEARCH
Open Access
Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats Hsiao-Chi Chuang1,2,3, Hsin-Chang Chen4, Pei-Jui Chai5, Ho-Tang Liao5, Chang-Fu Wu5,6, Chia-Ling Chen1, Ming-Kai Jhan7,8, Hui-I Hsieh9, Kuen-Yuh Wu5, Ta-Fu Chen10* and Tsun-Jen Cheng5,6*
Abstract Background: Epidemiological evidence has linked fine particulate matter (PM2.5) to neurodegenerative diseases; however, the toxicological evidence remains unclear. The objective of this study was to investigate the effects of PM2.5 on neuropathophysiology in a hypertensive animal model. We examined behavioral alterations (Morris water maze), lipid peroxidation (malondialdehyde (MDA)), tau and autophagy expressions, neuron death, and caspase-3 levels after 3 and 6 months of whole-body exposure to urban PM2.5 in spontaneously hypertensive (SH) rats. Results: SH rats were exposed to S-, K-, Si-, and Fe-dominated PM2.5 at 8.6 ± 2.5 and 10.8 ± 3.8 μg/m3 for 3 and 6 months, respectively. We observed no significant alterations in the escape latency, distance moved, mean area crossing, mean time spent, or mean swimming velocity after PM2.5 exposure. Notably, levels of MDA had significantly increased in the olfactory bulb, hippocampus, and cortex after 6 months of PM2.5 exposure (p < 0.05). We observed that 3 months of exposure to PM2.5 caused significantly higher expressions of t-tau and p-tau in the olfactory bulb (p < 0.05) but not in other brain regions. Beclin 1 was overexpressed in the hippocampus with 3 months of PM2.5 exposure, but significantly decreased in the cortex with 6 months exposure to PM2.5. Neuron numbers had decreased with caspase-3 activation in the cerebellum, hippocampus, and cortex after 6 months of PM2.5 exposure. Conclusions: Chronic exposure to low-level PM2.5 could accelerate the development of neurodegenerative pathologies in subjects with hypertension. Keywords: Air pollution, Autophagy, Central nervous system toxicity, Particulate matter, Tau
Background Particulate air pollution has been linked to initiation of neurodegenerative diseases (NGDs) [1, 2]. Results from an aging study cohort indicated that exposure to trafficrelated pollution and black carbon was associated with * Correspondence: [email protected]; [email protected] 10 Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, No. 1, Changde Street, Taipei 10048, Taiwan 5 Institute of Environmental and Occupational Health Science, College of Public Health, National Taiwan University, 17 Xu-Zhou Road, Taipei 100, Taiwan Full list of author information is available at the end of the article
decreases in cognition function [3]. Other results from the Nurses’ Health Study Cognitive Cohort in the US showed that exposure to coarse (with an aerodynamic diameter of 2.5 ~ 10 μm) (PM2.5–10) and fine (PM2.5) particulate matter size fractions was associated with cognitive declines [4]. Exposure to traffic-related air pollution was associated with an
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