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First published online June 5, 2008
Experimental Biology and Medicine 233:1081-1087 (2008)
doi: 10.3181/0712-RM-354
© 2008 by the Society for Experimental Biology and Medicine

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ORIGINAL RESEARCH ARTICLE

Regulatory Effects of Hydrogen Sulfide on IL-6, IL-8 and IL-10 Levels in the Plasma and Pulmonary Tissue of Rats with Acute Lung Injury

Tianshui Li*, Bin Zhao*,1, Cong Wang*, Haiying Wang*, Zhiwei Liu*, Wang Li{dagger}, Hongfang Jin{ddagger},§,2, Chaoshu Tang{dagger} and Junbao Du{ddagger},2

* Department of Emergency, Peking University Fourth Hospital, Beijing, China; {dagger} Health Science Center, Peking University, Beijing, China; {ddagger} Department of Pediatrics, Peking University First Hospital, Beijing, China; and § Key Lab of Molecular Cardiology, Ministry of Education of China, Beijing, China

To whom requests for reprints should be addressed at 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.

Key Words: hydrogen sulfide • acute lung injury • interleukin • polymorphonuclear







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