Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases · 2009
[The effect of nitric oxide inhalation on the expression of COX-2 and toll-like receptor 4 in rat acute lung injury induced by lipopolysaccharide].
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Wu Yan-wen, Bai Ming, Zhang Jian-chu, Jin Yang, Zhang Lei, Bao Bin
Аннотация
OBJECTIVE: To study the effect of nitric oxide (NO) on the expression of cyclo-oxygenase 2 (COX-2) and toll-like receptor 4 (TLR4) in a rat model of acute lung injury (ALI) induced by lipopolysaccharide (LPS).
METHODS: Twenty-four Sprague-Dawley rats were randomly divided into 4 groups. Group N: normal control group; Group L: ALI model by LPS intratracheal instillation; Group Za: ALI model+inhaled NO 20x10(-6) mg/L; Group Zb: ALI model+inhaled NO 100x10(-6) mg/L. Lung morphology was studied and COX-2 was detected by immunohistochemistry (IHC) while TLR4 by fluorescent quantitative PCR (FQ-PCR).
RESULTS: Immunohistochemistry and FQ-PCR showed that COX-2 (2.8+/-0.8) and TLR4 (2.1+/-0.7) were detected in the respiratory tract of the normal control rats. In Group L, the expression of COX-2 (6.5+/-2.8) and TLR4 (44.9+/-11.3) was increased in the main bronchus and bronchioles, compared to the normal controls (t=3.003, 10.480, both P<0.01). In Group Zb, the expression of COX-2 (5.0+/-2.0) and TLR4 (16.2+/-3.8) were decreased as compared to Group L, but only the level of TLR4 showed statistical difference (t=7.030, P<0.001).
CONCLUSIONS: COX-2 and TLR4 distributed widely in the respiratory tract of the rats. LPS increased the expression of COX-2 and TLR4. Low dose of nitric oxide (20x10(-6) mg/L) inhalation reduced the bronchiolar expression of COX-2 and TLR4 induced by LPS.
METHODS: Twenty-four Sprague-Dawley rats were randomly divided into 4 groups. Group N: normal control group; Group L: ALI model by LPS intratracheal instillation; Group Za: ALI model+inhaled NO 20x10(-6) mg/L; Group Zb: ALI model+inhaled NO 100x10(-6) mg/L. Lung morphology was studied and COX-2 was detected by immunohistochemistry (IHC) while TLR4 by fluorescent quantitative PCR (FQ-PCR).
RESULTS: Immunohistochemistry and FQ-PCR showed that COX-2 (2.8+/-0.8) and TLR4 (2.1+/-0.7) were detected in the respiratory tract of the normal control rats. In Group L, the expression of COX-2 (6.5+/-2.8) and TLR4 (44.9+/-11.3) was increased in the main bronchus and bronchioles, compared to the normal controls (t=3.003, 10.480, both P<0.01). In Group Zb, the expression of COX-2 (5.0+/-2.0) and TLR4 (16.2+/-3.8) were decreased as compared to Group L, but only the level of TLR4 showed statistical difference (t=7.030, P<0.001).
CONCLUSIONS: COX-2 and TLR4 distributed widely in the respiratory tract of the rats. LPS increased the expression of COX-2 and TLR4. Low dose of nitric oxide (20x10(-6) mg/L) inhalation reduced the bronchiolar expression of COX-2 and TLR4 induced by LPS.