Role of astrocyte activation in fine particulate matter-enhancement of existing ischemic stroke in Sprague-Dawley male rats.
Exposure to particulate matter (PM) with an aerodynamic diameter of less than 2.5 μm (PM2.5) is associated with increased risk of ischemic stroke, but potential neurotoxic mechanisms remain to be determined. In this study, adult male Sprague- Dawley (SD) rats were divided into four groups as follows: control (CON), PM2.5 exposure (PM alone), ischemic stroke (IS), and ischemic stroke and PM2.5 (IS-PM). Ischemic stroke groups were prepared by middle cerebral artery occlusion (MCAO), and neurobehavior was assessed daily for 7 consecutive days. The control group was administered intranasally 20 μl PBS, while PM2.5 alone was given as 20 μl of PM2.5 (10 mg/ml) intranasal daily for 7 consecutive days. The spontaneous locomotion and exploratory behavior of rats were assessed by the open field test. Cells positive for glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS) were determined for astrocyte activation and inflammatory reactions. Neuronal edema and pyknosis in the cerebral cortex, hippocampus, and midbrain were observed in IS groups with or without PM2.5 treatment. Astrocyte activity was enhanced, whereas spontaneous locomotion and exploratory movements decreased in the IS-PM group. Data demonstrated that astrocytes activation and inflammatory reactions may play a role in IS and that exposure to PM2.5 may aggravate the neurobehavioral alterations observed in rats suffering from IS.
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Chengcheng
C
Zhang
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Qingtao
Q
Meng
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Xin
X
Zhang
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Shenshen
S
Wu
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Shizhi
S
Wang
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Rui
R
Chen
a Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health , Southeast University , Nanjing 210009 , China.
Xiaobo
X
Li
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects* / Q000378:metabolism; D005106:Exploratory Behavior / Q000187:drug effects; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000139:chemically induced / Q000503:physiopathology*; D008124:Locomotion / Q000187:drug effects; D008297:Male; D055495:Neurogenesis / Q000187:drug effects; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
D000393:Air Pollutants; C000614142:Gfap protein, rat; D005904:Glial Fibrillary Acidic Protein; D052638:Particulate Matter; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat