[Effects of air mixed certain pollutants on the expression of CC16 and certain cytokine in pulmonary tissue of rats].
OBJECTIVE
To determine mRNA expressions of CC16, TNF-alpha and IL-6 in pulmonary tissue of rats exposed to air mixed pollutants and to explore mechanism of air pollutants on lung damage.


METHODS
48 Wistar rats were randomly divided into control group and three pollutant exposure groups. Pollutant exposure rats were intratracheally instillated contenting 15mg PM10 1ml physiological saline suspension and control group rats were intratracheally instillated 1ml physiological saline solution. Next day, three pollutant exposure groups rats were statically inhaled with mixed SO2 (15mg/m3), NO2 (12mg/m3), CO (400mg/m3) for 2h per day, and control group rats were inhaled with normal air. The expressions in pulmonary tissue of CC16, TNF-alpha and IL-6 mRNA were separately examined by RT-PCR, and the levels of CC16 in lung tissues and bronchoalveolar lavage fluids (BALF) were respectively measured by Immunohistochemistry and Western blotting after inhalation of mixed pollutants at the days of 1,7, and 30.


RESULTS
In rats inhaled with mixed pollutants, CC16 mRNA expressions of lung tissues significantly decreased at the days of 1, 7, and significantly increased at the days of 30. TNF-alpha and IL-6 mRNA expressions of lung tissues in rats inhaled with mixed pollutants at the days of 1, 7 were more higher than those of control groups. At the days of 30, TNF-alpha and IL-6 mRNA expressions of lung tissues decreased again. Immunohistochemistry results showed that CC16 expressions in lung tissues were significantly higher than those of control groups at the days of 1, 7, and significantly decreased at the days of 30. The levels of CC16 in BALF at the days of 1, 7 were lower than those of control groups and at the days of 30.


CONCLUSIONS
The expression levels of CC16 in lung tissues and BALF could decrease and TNF-alpha and IL-6 expressions could increase of lung tissues in rats inhaled with mixed pollutants at early stage of exposure pollutants.
Xiao
Chunling
C
School of Public Health, Shenyang Medical College, Shenyang 110034, China.
Guo
Li
L
Qi
Rong
R
Xi
Shuhua
S
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D002248:Carbon Monoxide / Q000633:toxicity; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000378:metabolism*; D008297:Male; D009585:Nitrogen Dioxide / Q000633:toxicity; D052638:Particulate Matter / Q000633:toxicity*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013458:Sulfur Dioxide / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D014598:Uteroglobin / Q000235:genetics / Q000378:metabolism*
D000393:Air Pollutants; D016207:Cytokines; D015850:Interleukin-6; D052638:Particulate Matter; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D013458:Sulfur Dioxide; D002248:Carbon Monoxide; D014598:Uteroglobin; D009585:Nitrogen Dioxide