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

被引:27
作者
Xu, Dun-quan [1 ]
Gao, Cao [2 ]
Niu, Wen [1 ]
Li, Yan [3 ]
Wang, Yan-xia [1 ]
Gao, Chang-jun [2 ]
Ding, Qian [2 ]
Yao, Li-nong [2 ]
Chai, Wei [2 ]
Li, Zhi-chao [1 ]
机构
[1] Fourth Mil Med Univ, Dept Pathol & Pathophysiol, Xian 710038, Peoples R China
[2] Fourth Mil Med Univ, Tangdu Hosp, Dept Anesthesiol, Xian 710038, Peoples R China
[3] Beijing Mil Gen Hosp, Med Examinat Ctr, Beijing 100007, Peoples R China
基金
中国国家自然科学基金;
关键词
hemorrhagic shock; lung injury; inflammation; oxidative stress; apoptosis; Fas/FasL; hydrogen sulfide; sodium hydrosulfide; HYDROGEN-SULFIDE PROTECTS; OXIDATIVE STRESS; SUSPENDED ANIMATION; FAS LIGAND; INJURY; DEATH; EXPRESSION; ISCHEMIA; MECHANISM; DONOR;
D O I
10.1038/aps.2013.96
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Aim: 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 mu mol/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-alpha, 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 center dot 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.
引用
收藏
页码:1515 / 1525
页数:11
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