Effects of Hhydrogen Sulfide on the Inflammatory Reaction and the Expression of Single Immunoglobin IL-1 Receptor Related Protein in Rats with Acute Lung Injury Induced by Lipopolysaccharide
10.11969/j.issn.1673-548X.2018.02.011
- VernacularTitle:硫化氢对大鼠内毒性急性肺损伤炎性反应及单免疫球蛋白白介素-1相关蛋白表达的影响
- Author:
Zhihai HAN
1
;
Jiguang MENG
;
Xuxin CHEN
Author Information
1. 中国人民解放军海军总医院呼吸内科
- Keywords:
Hydrogen sulfide;
Lipopolysaccharide;
Acute lung injury;
Inflammation;
Single immunoglobin IL-1 receptor related protein
- From:
Journal of Medical Research
2018;47(2):41-44,52
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effects of hydrogen sulfide (H2 S) on the inflammatory reaction and the expression of single immunoglobin IL-1 receptor related protein (SIGIRR) in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS). Methods Forty male SD rats were randomly divided into 4 groups (normal group, H2 S group, ALI group and ALI + H2 S group). The ALI rat model was established by LPS peritoneal injection. After LPS stimulation for 1 h, rats inhaled H2 S 80mg /m3 for 6h. Then, rats were sacrificed with a supraphysiological dose of pentobarbital sodium. The histological changes in the lung, the levels of TNF-α and IL-1β in serum and lung tissue homogenates, and the protein expression of SIGIRR in lung tissues were examined. Results Compared with the normal and H2 S groups, typical histological features of ALI were observed in ALI group, and the lung injury scores of ALI group were higher than those of the normal and H2 S groups (P ＜ 0. 05). Moreover, there were marked increases in the levels of TNF-α and IL-1β in serum and lung tissue homogenates after LPS injection. In contrast, inhalation of H2 S could attenuate lung pathological changes and inhibit the productions of TNF-α and IL-1β in serum and lung tissue homogenates (P ＜ 0. 05). Additionally, inhalation of H2 S could induce the protein expression of SIGIRR in rat lung tissues. Conclusion Inhalation of H2 S protected rats from LPS-induced ALI and its mechanisms were partially associated with inhibition of the productions of TNF-α and IL-1β and modulation of SIGIRR expression.
