Effects of sulfur dioxide on the expressions of EGF, EGFR, and COX-2 in airway of asthmatic rats.
The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that SO(2)might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to SO(2), male Wistar rats were divided randomly into four equal groups of six animals each: (1) SO(2) group, (2) ovalbumin (OVA) group (asthma group), (3) SO(2)plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or SO(2) (5.6 mg/m(3)) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription-polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled SO(2) alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus SO(2) inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that SO(2) could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which SO(2) pollution aggravates asthma disease.
Li
Ruijin
R
Research Center of Environmental Science and Engineering and Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan, 030006, China.
Meng
Ziqiang
Z
Xie
Jingfang
J
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D004357:Drug Synergism; D004815:Epidermal Growth Factor / Q000235:genetics / Q000378:metabolism*; D066246:ErbB Receptors / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects; D019570:Inhalation Exposure; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010047:Ovalbumin / Q000276:immunology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013458:Sulfur Dioxide / Q000633:toxicity*; D014132:Trachea / Q000187:drug effects / Q000378:metabolism
D000393:Air Pollutants; D012333:RNA, Messenger; D013458:Sulfur Dioxide; D004815:Epidermal Growth Factor; D010047:Ovalbumin; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; C483803:Egfr protein, rat; D066246:ErbB Receptors