ArticleEuropean journal of medical research2017
Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats.
Article in European journal of medical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Rapamycin inhibits LOC102553434-mediated pyroptosis to improve lung injury induced by limb ischemia-reperfusion.3 Biotech · 2021Article
- Electroacupuncture pre‑conditioning protects from lung injury induced by limb ischemia/reperfusion through TLR4 and NF‑κB in rats.Molecular medicine reports · 2020Article
- Protective Effects of Ischemic Postconditioning on Livers in Rats with Limb Ischemia-Reperfusion via Glycogen Synthase Kinase 3 beta (GSK-3β)/Fyn/Nuclear Receptor-Erythroid-2-Related Factor (Nrf2) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Electro-Acupuncture on ST36 and SP6 Acupoints Ameliorates Lung Injury via Sciatic Nerve in a Rat Model of Limb Ischemia-Reperfusion.Journal of inflammation research · 2020Article
- Protective effects of HO-1 pathway on lung injury subsequent to limb ischemia reperfusion.The Kaohsiung journal of medical sciences · 2019Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats.
methodsALI was induced by bilateral hind limb I/R in Sprague-Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis.
resultsLimb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate.
conclusionCarbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.
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