Journal of pediatric surgery · 2016
Intestinal epithelial cell injury is rescued by hydrogen sulfide.
СтатьяНазвание и аннотация: Перевод в очереди
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Li Bo, Zani Augusto, Martin Zechariah, Lee Carol, Zani-Ruttenstock Elke, Eaton Simon, Pierro Agostino
Аннотация
BACKGROUND/PURPOSE: Oxidative stress is implicated in the pathogenesis of necrotizing enterocolitis (NEC). Hydrogen sulfide (H2S) has been reported to have a protective function against oxidative stress in the gut. We hypothesize that administration of H2S can help decrease intestinal epithelial cell injury in vitro.
METHODS: Intestinal epithelial cells (IEC-18) were treated with 200μM hydrogen peroxide (H2O2) for 21h. At 21h sodium hydrosulfide (NaHS), an H2S donor, was administered as a rescue treatment at two different concentrations: 0.1mM and 0.2mM. At 24h, cell viability was measured using a colorimetric assay (MTT). Oxidative stress was studied by glutathione peroxidase (GPx) activity and thiobarbituric acid reactive substances (TBARS). IL-6 and TNFα levels were tested to study inflammation. Data were presented as mean±SD and compared using one-way ANOVA with Bonferroni post-test.
RESULTS: Compared to control, H2O2-treated IEC-18 had reduced viability (p<0.01), lower GPx activity (p<0.01), higher TBARS levels (p<0.01), and increased IL6 and TNFα (p<0.001). Compared to H2O2-treated IEC-18, treatment with 0.2mM NaHS rescued viability (p<0.01), increased GPx activity (p<0.05), and reduced TBARS (p<0.01), IL6 and TNFα (p<0.001).
CONCLUSIONS: H2S successfully rescues epithelial cell damage induced by oxidative stress in vitro. This indicates that H2S could be a potential pharmacological intervention in conditions like NEC.
METHODS: Intestinal epithelial cells (IEC-18) were treated with 200μM hydrogen peroxide (H2O2) for 21h. At 21h sodium hydrosulfide (NaHS), an H2S donor, was administered as a rescue treatment at two different concentrations: 0.1mM and 0.2mM. At 24h, cell viability was measured using a colorimetric assay (MTT). Oxidative stress was studied by glutathione peroxidase (GPx) activity and thiobarbituric acid reactive substances (TBARS). IL-6 and TNFα levels were tested to study inflammation. Data were presented as mean±SD and compared using one-way ANOVA with Bonferroni post-test.
RESULTS: Compared to control, H2O2-treated IEC-18 had reduced viability (p<0.01), lower GPx activity (p<0.01), higher TBARS levels (p<0.01), and increased IL6 and TNFα (p<0.001). Compared to H2O2-treated IEC-18, treatment with 0.2mM NaHS rescued viability (p<0.01), increased GPx activity (p<0.05), and reduced TBARS (p<0.01), IL6 and TNFα (p<0.001).
CONCLUSIONS: H2S successfully rescues epithelial cell damage induced by oxidative stress in vitro. This indicates that H2S could be a potential pharmacological intervention in conditions like NEC.