Fangyan Wang1, Zengyou Jin2, Kaiyi Shen3, Tingting Weng3, Zhisong Chen3, Jiahui Feng3, Zhengzheng Zhang3, Jiaming Liu4, Xiaolong Zhang5, Maoping Chu6. 1. Department of Pathophysiology, Wenzhou Medical University, Zhejiang Province, China; Children's Heart Center, The Second Affiliated Hospital & Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Zhejiang Province, China. 2. Department of Pediatrics of The First Affiliated Hospital, Wenzhou Medical University, Zhejiang Province, China. 3. Department of Pathophysiology, Wenzhou Medical University, Zhejiang Province, China. 4. School of Environmental Science and Public Health, Wenzhou Medical University, Zhejiang Province, China. Electronic address: wzljm@wzmc.edu.cn. 5. Department of Intensive Care Unit of The Second Affiliated Hospital, Wenzhou Medical University, Zhejiang Province, China. 6. Children's Heart Center, The Second Affiliated Hospital & Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Zhejiang Province, China. Electronic address: chmping@hotmail.com.
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 3days prior to LPS administration (30 mg/kg). Normal group received saline only. 6h and 12h 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<0.01) 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<0.01). 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<0.01 or P<0.05). CONCLUSIONS: In conclusion, pretreatment with butyrate attenuated septic heart depression via anti-inflammation and anti-oxidation.
OBJECTIVES: The depressed heart function is the main complication to cause death of septicpatients 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 3days prior to LPS administration (30 mg/kg). Normal group received saline only. 6h and 12h 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<0.01) 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<0.01). 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<0.01 or P<0.05). CONCLUSIONS: In conclusion, pretreatment with butyrateattenuated septic heart depression via anti-inflammation and anti-oxidation.