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

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 CA-treated rats compared to controls. Administration of the H2S donor sodium hydrosulfide (NaHS, 56 mu mol/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.