title: Seasonal variation in air particulate matter (PM10) exposure-induced ischemia-like injuries in the rat brain.
abstract: Epidemiological studies imply a significantly positive association between particulate matter (PM) level and ischemic stroke hospitalization. However, considering that PM10 is highly heterogeneous and varies with season within the same location, existing experimental evidence remained low. In the present study, we first treated Wistar rats with PM10 samples collected from different seasons in Taiyuan, a typically coal-burning city of China, and determined ischemia-related markers in the cortex. The results indicated that PM10 exposure caused endothelial dysfunction, inflammatory response, and neuro-functional impairment similar to that of cerebral ischemia with season-dependent properties, and the winter sample presented the most obvious injuries. Then, we detected the chemical composition of PM10 samples followed by analysis of their correlation with the above biomarkers and found that winter PM10, characterized by higher polycyclic aromatic hydrocarbons (PAHs) and carbon load, played the major role in causing brain ischemia-like injuries among different season samples. Furthermore, by setting up an ischemic neuron model in vitro, we confirmed that winter PM10 presented the most serious aggravation on ischemia-produced injury outcome. This study provides experimental evidence for clarifying the association between season-dependent PM10 pollution in the atmospheric environment and an increased risk of ischemia-like injuries.
authors.affiliation: College of Environment and Resource, Research Center of Environment and Health, Shanxi University , Taiyuan, Shanxi 030006, P. R. China.
authors.forename: Lin
authors.initials: L
authors.lastname: Guo
authors.forename: Ben
authors.initials: B
authors.lastname: Li
authors.forename: Juan-Juan
authors.initials: JJ
authors.lastname: Miao
authors.forename: Yang
authors.initials: Y
authors.lastname: Yun
authors.forename: Guang-Ke
authors.initials: GK
authors.lastname: Li
authors.forename: Nan
authors.initials: N
authors.lastname: Sang
mesh_terms: D000280:Administration, Inhalation; D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000139:chemically induced* / Q000378:metabolism; D002244:Carbon / Q000032:analysis / Q000633:toxicity; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D019332:Endothelin-1 / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D008670:Metals / Q000032:analysis / Q000633:toxicity; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000235:genetics / Q000378:metabolism; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis / Q000633:toxicity; D012333:RNA, Messenger / Q000378:metabolism; D017208:Rats, Wistar; D012621:Seasons
chemical_list: D000393:Air Pollutants; D019332:Endothelin-1; D053583:Interleukin-1beta; D008670:Metals; D052638:Particulate Matter; D011084:Polycyclic Aromatic Hydrocarbons; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D002244:Carbon; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat