Pulmonary responses to fine particles: differences between the spontaneously hypertensive rats and wistar kyoto rats.
In order to explore the potential mechanism that animals with cardiopulmonary diseases were more susceptible than healthy animals, the spontaneously hypertensive rats (SHR) as a model of human cardiovascular disease were used. SHR and wistar kyoto rats (WKY) were exposed by intratracheal instillation to fine particles with the doses of 0.0 (saline), 1.6, 8.0 and 40.0mg/kg body weight, respectively. The exposure was done once a day, for three continuous days. The rats were killed after 24h following the last exposure, followed by analysis of bronchoalveolar lavage fluid (BALF) to estimate the lung injury. Meantime, parameters of oxidative stress, cytokines and cell surface receptors related to inflammation and anti-inflammation were also measured. The results showed that lactate dehydrogenase (LDH) activity, percentages of neutrophils and lymphocytes, and expression of TBA-reactive substances and cytokines (IL-1beta, TNF-alpha, MIP-2, OPN, NF-kappaB, CC16 and HO-1) and cell surface receptors (CD44 and TLR-4) were increased in rats, but percentage of macrophages decreased. Meanwhile, at the same dose exposed, the levels of those parameters were higher in SHR than that in WKY rats. The results indicated that inflammation might be one of the mechanisms of lung injury induced by fine particles. Results of comparisons of different response to fine particles between SHR and WKY rats suggested that lung injury induced by fine particles was greater in SHR than that in WKY rats.
Cao
Qiang
Q
Department of Environment Health, School of Public Health, Fudan University, Shanghai 200032, China.
Zhang
Shu
S
Dong
Chen
C
Song
Weimin
W
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D016207:Cytokines / Q000096:biosynthesis; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000378:metabolism; D007150:Immunohistochemistry; D007958:Leukocyte Count; D008168:Lung / Q000187:drug effects*; D008171:Lung Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology*; D018655:Lymphocyte Count; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D052638:Particulate Matter / Q000633:toxicity*; D011014:Pneumonia / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011956:Receptors, Cell Surface / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013045:Species Specificity; D013535:Suspensions; D051996:Transcription Factor RelA / Q000096:biosynthesis
D016207:Cytokines; D052638:Particulate Matter; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D013535:Suspensions; D051996:Transcription Factor RelA; D051547:Heme Oxygenase-1; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases