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ORIGINAL RESEARCH ARTICLE |


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* Department of Emergency, Peking University Fourth Hospital, Beijing, China;
Health Science Center, Peking University, Beijing, China;
Department of Pediatrics, Peking University First Hospital, Beijing, China; and
Key Lab of Molecular Cardiology, Ministry of Education of China, Beijing, China
2 Department of Pediatrics, Peking University First Hospital, West District, Beijing 100034, China. E-mail: junbaodu1{at}126.com; jinhongfang51{at}126.com
We examined the possible role of hydrogen sulfide (H2S) in the pathogenesis of oleic acid (OA)-induced acute lung injury (ALI) and its regulatory effects on the inflammatory response. Compared to control rats, the OA-treated rats had decreased partial pressure of oxygen in the arterial blood (PaO2) levels, an increased pulmonary wet/dry weight (W/D) ratio, increased index of quantitative assessment (IQA) score and increased frequency of polymorphonuclear (PMN) cells in the lung 2, 4 or 6 h after OA injection (0.1 ml/kg, intravenous injection). In addition, significantly increased IL-6, IL-8 and IL-10 levels together with decreased H2S levels were observed in the plasma and lung tissue of OA-treated rats compared to controls. Administration of the H2S donor sodium hydrosulfide (NaHS, 56 µmol/L, intraperitoneal injection) into OA-treated rats increased the PaO2 level, reduced the lung W/D ratio and infiltration of PMN cells, and alleviated the degree of ALI (measured by the IQA score). In addition, NaHS decreased IL-6 and IL-8 levels but increased IL-10 levels in the plasma and lung tissues, suggesting that H2S may regulate the inflammatory response during ALI via regulation of IL-6, IL-8 and IL-10. Thus, the down-regulation of endogenous H2S production might be involved in the pathogenesis of OA-induced ALI in rats.
Keywords: hydrogen sulfide, acute lung injury, interleukin, polymorphonuclear
This work was supported by the National Natural Science Foundation of China (30630031), the National Science Fund for Distinguished Young Scholars (30425010), the Major Basic Research Program of China (2006CB503807), and the Beijing Natural Science Foundation (7072082 and 7082095).
1 Co-first authors: Tianshui Li and Bin Zhao contributed equally to this work.
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