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Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2020-11-26 , DOI: 10.1186/s12989-020-00388-6
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

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. 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. Chronic exposure to low-level PM2.5 could accelerate the development of neurodegenerative pathologies in subjects with hypertension.

中文翻译:

自发性高血压大鼠在3个月和6个月的低水平PM 2.5吸入暴露下会改变神经病理学

流行病学证据表明,细颗粒物(PM2.5)与神经退行性疾病有关。然而,毒理学证据仍不清楚。这项研究的目的是调查高血压动物模型中PM2.5对神经病理生理的影响。我们检查了全身性自发性高血压患者暴露于城市PM2.5 3和6个月后的行为改变(莫里斯水迷宫),脂质过氧化(丙二醛(MDA)),tau和自噬表达,神经元死亡和caspase-3水平。 (SH)大鼠。SH大鼠分别以8.6±2.5和10.8±3.8μg/ m3的S-,K-,Si-和Fe为主的PM2.5暴露3个月和6个月。我们观察到,PM2.5暴露后的逃生潜伏期,移动距离,平均穿越面积,平均花费时间或平均游泳速度没有明显变化。值得注意的是 PM2.5暴露6个月后,嗅球,海马和皮层的MDA水平显着增加(p <0.05)。我们观察到,暴露于PM2.5的3个月会导致嗅球中t-tau和p-tau的表达明显升高(p <0.05),但在其他脑区域则没有。Beclin 1在PM2.5暴露3个月后在海马中过表达,但在PM2.5暴露6个月后在皮质中明显降低。PM2.5暴露6个月后,小脑,海马和皮层中caspase-3的激活使神经元数量减少。长期暴露于低水平的PM2.5可能会加速高血压患者神经退行性病变的发展。我们观察到,暴露于PM2.5的3个月会导致嗅球中t-tau和p-tau的表达明显升高(p <0.05),但在其他脑区域则没有。Beclin 1在PM2.5暴露3个月后在海马中过表达,但在PM2.5暴露6个月后在皮质中明显降低。PM2.5暴露6个月后,小脑,海马和皮层中caspase-3的激活使神经元数量减少。长期暴露于低水平的PM2.5可能会加速高血压患者神经退行性病变的发展。我们观察到,暴露于PM2.5的3个月会导致嗅球中t-tau和p-tau的表达明显升高(p <0.05),但在其他脑区域则没有。Beclin 1在PM2.5暴露3个月后在海马中过表达,但在PM2.5暴露6个月后在皮质中明显降低。PM2.5暴露6个月后,小脑,海马和皮层中caspase-3的激活使神经元数量减少。长期暴露于低水平的PM2.5可能会加速高血压患者神经退行性病变的发展。但暴露于PM2.5的6个月后皮质中显着减少。PM2.5暴露6个月后,小脑,海马和皮层中caspase-3的激活使神经元数量减少。长期暴露于低水平的PM2.5可能会加速高血压患者神经退行性病变的发展。但暴露于PM2.5的6个月后皮质中显着减少。PM2.5暴露6个月后,小脑,海马和皮层中caspase-3的激活使神经元数量减少。长期暴露于低水平的PM2.5可能会加速高血压患者神经退行性病变的发展。
更新日期:2020-11-27
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