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

Abstract

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 micromol/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.

Roles of the Exogenous H2S-Mediated SR-A Signaling Pathway in Renal Ischemia/ Reperfusion Injury in Regulating Endoplasmic Reticulum Stress-Induced Autophagy in a Rat Model

“…IL-6 is closely associated with inflammation, suggesting that SR-A deficiency may negatively affect the expression of IL-6 and TGF-β [38]. H 2 S has been reported to be involved in the negative regulation of inflammatory responses related to a variety of cytokines, thus suggesting that H 2 S has the potential to decrease IL-6 and TGF-β [39]. The findings of Wang et al suggested that SR-A gene knockout protects mice from progressive nephropathy by suppressing the TGF-β pathway [33].…”

The therapeutic potential of hydrogen sulfide: separating hype from hope

“…Plasma H 2 S is reported to decrease in rats with oelic acidinduced lung injury; exogenous H 2 S increases arterial Pa O 2 , decreases pulmonary edema and infiltration of polymorphonuclear cells, decreases IL-6 and IL-8, but increases IL-10, suggesting that endogenous H 2 S production is decreased in this model of lung injury (93). CSE expression in airway and vascular smooth muscle decreases in ovalbumin-induced lung asthma, whereas exogenous H 2 S alleviates inflammation, restores expiratory flow, and attenuates iNOS activation (22).…”

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

“…Hydrogen sulfide (H 2 S) has also recently been shown to be an important mediator of inflammatory responses and may induce the production or release of substance P [89,90]. Although H 2 S may be proinflammatory, in certain models of ALI, H 2 S production is decreased, and administration of the H 2 S donor sodium hydrosulfide decreased proinflammatory cytokines IL-6 and IL-8, and the resultant ALI [91]. Thus, further studies are needed to better define the interplay of H 2 S and substance P in mediating ALI.…”