ArticleActa pharmacologica Sinica2013
Sodium hydrosulfide alleviates lung inflammation and cell apoptosis following resuscitated hemorrhagic shock in rats.
Article in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Doxycycline reduces liver and kidney injuries in a rat hemorrhagic shock model.Intensive care medicine experimental · 2024Article
- Innate immunity and immunotherapy for hemorrhagic shock.Frontiers in immunology · 2022Review
- Protective effect of hydrogen sulfide against stress-induced lung injury: involvement of Nrf2, NFκB/iNOS, and HIF-1α signaling pathways.Cell stress & chaperones · 2022Article
- Hydrogen Sulfide Inhibits TMPRSS2 in Human Airway Epithelial Cells: Implications for SARS-CoV-2 Infection.Biomedicines · 2021Article
- The Role of Hydrogen Sulfide in Respiratory Diseases.Biomolecules · 2021Review
- Understanding hydrogen sulfide signaling in neonatal airway disease.Expert review of respiratory medicine · 2021Review
- Hydrogen Sulfide and its Interaction with Other Players in Inflammation.Advances in experimental medicine and biology · 2021Article
- Medullary Noradrenergic Neurons Mediate Hemodynamic Responses to Osmotic and Volume Challenges.Frontiers in physiology · 2021Article
- HAmerican journal of physiology. Cell physiology · 2020Review
- Involvement of median preoptic nucleus and medullary noradrenergic neurons in cardiovascular and sympathetic responses of hemorrhagic rats.Scientific reports · 2018Article
- Anti-inflammatory effects of HJournal of translational medicine · 2017Review
- The anti-inflammatory effect of hydrogen sulphide on acute necrotizing pancreatitis in rats.Turkish journal of surgery · 2017Article
- Hydrogen Sulfide Is an Antiviral and Antiinflammatory Endogenous Gasotransmitter in the Airways. Role in Respiratory Syncytial Virus Infection.American journal of respiratory cell and molecular biology · 2016Article
- Delayed Treatment with Sodium Hydrosulfide Improves Regional Blood Flow and Alleviates Cecal Ligation and Puncture (CLP)-Induced Septic Shock.Shock (Augusta, Ga.) · 2016Article
- Role of hydrogen sulfide in paramyxovirus infections.Journal of virology · 2015Article
- An exogenous hydrogen sulphide donor, NaHS, inhibits the apoptosis signaling pathway to exert cardio-protective effects in a rat hemorrhagic shock model.International journal of clinical and experimental pathology · 2015Article
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- A novel controllable hydrogen sulfide-releasing molecule protects human skin keratinocytes against methylglyoxal-induced injury and dysfunction.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2014Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the protective effects of hydrogen sulfide (H2S) against inflammation, oxidative stress and apoptosis in a rat model of resuscitated hemorrhagic shock.
methodsHemorrhagic 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.
resultsResuscitated 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.
conclusionNaHS administration protects rat lungs against inflammatory responses induced by resuscitated hemorrhagic shock via suppressing oxidative stress and the Fas/FasL apoptotic signaling pathway.
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