Hydrogen Sulfide Exerts Anti-oxidative and Anti-inflammatory Effects in Acute Lung Injury

Abstract

Acute lung injury (ALI) caused by septic stimuli is still a major problem in critical care patients. We have shown previously that hydrogen sulfide (HS) mediates anti-inflammatory and lung protective effects. In the present study, we aimed to investigate the underlying mechanisms. C57BL/6N mice were instilled with lipopolysaccharide (LPS) intranasally in the absence or presence of inhaled HS for 6 h. LPS instillation led to alveolar wall thickening, an elevated ALI score, increased neutrophil transmigration, and elevated interleukin-1β cytokine release into the bronchoalveolar lavage fluid. In contrast, HS inhalation prevented lung injury and inflammation despite LPS treatment. Moreover, HS inhalation significantly inhibited protein expression of cystathionine-β-synthetase, heat shock protein 70, phosphorylated p38 MAP kinase, NADPH oxidase 2, and the formation of reactive oxygen species (ROS) in LPS-challenged animals. In conclusion, HS prevents LPS-induced ALI by inhibition of pro-inflammatory and oxidative responses via the concerted attenuation of stress protein, MAP kinase, and ROS signaling pathways.

High levels of dietary methionine improves sitagliptin-induced hepatotoxicity by attenuating oxidative stress in hypercholesterolemic rats

“…Additionally, cysteine (cys) which is an intermediate in this pathway, serves as the precursor for the formation of glutathione which is the most potent biological antioxidant. Both cystine (the disulfide of cys) and cystathionine are also the sources for the formation of hydrogen sulfide, a gaseous molecule which has been shown to have anti-oxidative, vasodilatory and antiinflammatory properties in addition to several other benefits [67,68]. Most importantly, Met by itself has been shown to have anti-oxidative properties [32,45,47].…”

Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury

“…In order to evaluate possible (pre)treatment options, we and others have previously shown that inhalation of hydrogen sulfide (H 2 S) prevents neutrophil accumulation in models of ventilator- 7 – 9 and lipopolysaccharide (LPS)-induced lung injury 10 – 14 . Although recent data suggest that H 2 S may limit neutrophil activation and transmigration by downregulating pulmonary expression of chemoattractant molecules 15 or by reducing leukocyte rolling and adhesion 15 – 18 , it remains completely unknown how H 2 S interacts with the neutrophilic inflammatory response.…”

Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle

“…In mice, absence of CSE expression promotes AHR. 29 Exogenous administration of H 2 S has been demonstrated as protective in ventilator-induced lung injury, 68,69 acute lung injury, [70][71][72][73][74] hypoxia/hyperoxia environments, [74][75][76] and during acute viral illnesses. [77][78][79] Compared to these data, there is currently no information on H 2 S in the developing bronchial airways per se.…”