Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats

  • Hsiao-Chi Chuang (Contributor)
  • Hsin Chang Chen (Creator)
  • Pei-Jui Chai (Contributor)
  • Ho-Tang Liao (Contributor)
  • Chang fu Wu (Creator)
  • Chia-Ling Chen (Creator)
  • Ming Kai Jhan (Creator)
  • Hui I. Hsieh (Contributor)
  • Kuen Yuh Wu (Creator)
  • Ta Fu Chen (Creator)
  • Tsun Jen Cheng (Contributor)



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
Date made available2020

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