Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats
Hsiao‐Chi Chuang, Hsin‐Chang Chen, Pei-Jui Chai, Ho‐Tang Liao, Chang‐Fu Wu, Chia‐Ling Chen, Ming-Kai Jhan, Hui-I Hsieh, Kuen‐Yuh Wu, Ta‐Fu Chen, Tsun‐Jen Cheng
Abstract
Abstract Background Epidemiological evidence has linked fine particulate matter (PM 2.5 ) to neurodegenerative diseases; however, the toxicological evidence remains unclear. The objective of this study was to investigate the effects of PM 2.5 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 PM 2.5 in spontaneously hypertensive (SH) rats. Results SH rats were exposed to S-, K-, Si-, and Fe-dominated PM 2.5 at 8.6 ± 2.5 and 10.8 ± 3.8 μg/m 3 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 PM 2.5 exposure. Notably, levels of MDA had significantly increased in the olfactory bulb, hippocampus, and cortex after 6 months of PM 2.5 exposure ( p < 0.05). We observed that 3 months of exposure to PM 2.5 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 PM 2.5 exposure, but significantly decreased in the cortex with 6 months exposure to PM 2.5 . Neuron numbers had decreased with caspase-3 activation in the cerebellum, hippocampus, and cortex after 6 months of PM 2.5 exposure. Conclusions Chronic exposure to low-level PM 2.5 could accelerate the development of neurodegenerative pathologies in subjects with hypertension.