Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti -inflammation and anti -oxidation
Abstract Objectives The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the under...
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Veröffentlicht in: | The American journal of emergency medicine 2017-03, Vol.35 (3), p.402-409 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Objectives The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism. Methods Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3 days prior to LPS administration (30 mg/kg). Normal group received saline only. 6 h and 12 h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis. Results The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P < .01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P < .01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P < .01 or P < .05). Conclusions In conclusion, pretreatment with butyrate attenuated septic heart depression via anti -inflammation and anti-oxidation. |
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ISSN: | 0735-6757 1532-8171 |
DOI: | 10.1016/j.ajem.2016.11.022 |