Sodium hydrosulfide alleviates lung inflammation and cell apoptosis following resuscitated hemorrhagic shock in rats

Abstract

Aim: To investigate the protective effects of hydrogen sulfide (H 2 S) against inflammation, oxidative stress and apoptosis in a rat model of resuscitated hemorrhagic shock. Methods: Hemorrhagic shock was induced in adult male SD rats by drawing blood from the femoral artery for 10 min. The mean arterial pressure was maintained at 35-40 mmHg for 1.5 h. After resuscitation the animals were observed for 200 min, and then killed. The lungs were harvested and bronchoalveolar lavage fluid was prepared. The levels of relevant proteins were examined using Western blotting and immunohistochemical analyses. NaHS (28 μmol/kg, ip) was injected before the resuscitation. Results: Resuscitated hemorrhagic shock induced lung inflammatory responses and significantly increased the levels of inflammatory cytokines IL-6, TNF-α, and HMGB1 in bronchoalveolar lavage fluid. Furthermore, resuscitated hemorrhagic shock caused marked oxidative stress in lung tissue as shown by significant increases in the production of reactive oxygen species H 2 O 2 and ·OH, the translocation of Nrf2, an important regulator of antioxidant expression, into nucleus, and the decrease of thioredoxin 1 expression. Moreover, resuscitated hemorrhagic shock markedly increased the expression of death receptor Fas and Fas-ligand and the number apoptotic cells in lung tissue, as well as the expression of pro-apoptotic proteins FADD, active-caspase 3, active-caspase 8, Bax, and decreased the expression of Bcl-2. Injection with NaHS significantly attenuated these pathophysiological abnormalities induced by the resuscitated hemorrhagic shock. Conclusion: NaHS administration protects rat lungs against inflammatory responses induced by resuscitated hemorrhagic shock via suppressing oxidative stress and the Fas/FasL apoptotic signaling pathway.

The anti-inflammatory effect of hydrogen sulphide on acute necrotizing pancreatitis in rats

“…Coagulopathies in microcirculation, lipase and phospholipase activities; and arteriovenous shunts opened by the release of kinines are the triggering factors leading to the development of ARDS (33). In the present study, LDH in BAL fluid and MDH Xu et al (14) Showed that H 2 S prevents lung injury, inhibits apoptosis and decreases inflammatory response in hemorrhagic shock-induced rats. Also, in a study by Lıu et al (39) it was reported that H 2 S inhibits Fas pathway and has preventive effectsin acute lung injury-induced rats.…”

“…NaHS addition did not show any decrease in IL-6 levels. However, Xu et al (14) showed that H 2 S inhibits TNF-α and IL-6 in their study.…”

“…In the present study, we did not work on apoptosis. Xu DQ et al (14) showed the antiapoptotic property of H 2 S in their study.…”

“…However, in this study, the anti-inflammatory effect of H 2 S was observed by comparing the effects of H 2 S-releasing NSAID (diclophenac) and H 2 S-non-releasing NSAID (14). H 2 S-releasing drugs were shown to have anti-inflammatory effects (28).…”

“…The anti-inflammatory effect of H 2 S was also shown by the inhibition of TNF-α vs. IL-6 in the study of Xu et al (14) with hemorrhagic shock-induced rats. H 2 S inhibits the nuclear factor κβ (NF-κβ), one of the main regulators of inflammation, and decreases proinflammatory cytokines, chemokines, and adhesion molecules (15)(16)(17).…”