title: Sodium hydrosulfide alleviates lung inflammation and cell apoptosis following resuscitated hemorrhagic shock in rats.
abstract: OBJECTIVE
  To investigate the protective effects of hydrogen sulfide (H2S) 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 H2O2 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.
  
  
  CONCLUSIONS
  NaHS administration protects rat lungs against inflammatory responses induced by resuscitated hemorrhagic shock via suppressing oxidative stress and the Fas/FasL apoptotic signaling pathway.
authors.affiliation: Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi-an 710032, China.
authors.forename: Dun-quan
authors.initials: DQ
authors.lastname: Xu
authors.forename: Cao
authors.initials: C
authors.lastname: Gao
authors.forename: Wen
authors.initials: W
authors.lastname: Niu
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.forename: Yan-xia
authors.initials: YX
authors.lastname: Wang
authors.forename: Chang-jun
authors.initials: CJ
authors.lastname: Gao
authors.forename: Qian
authors.initials: Q
authors.lastname: Ding
authors.forename: Li-nong
authors.initials: LN
authors.lastname: Yao
authors.forename: Wei
authors.initials: W
authors.lastname: Chai
authors.forename: Zhi-chao
authors.initials: ZC
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001992:Bronchoalveolar Lavage Fluid; D008297:Male; D011014:Pneumonia / Q000150:complications / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000150:complications*; D013440:Sulfides / Q000494:pharmacology*
chemical_list: D013440:Sulfides; C025451:sodium bisulfide