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中华损伤与修复杂志(电子版) ›› 2017, Vol. 12 ›› Issue (03) : 223 -227. doi: 10.3877/cma.j.issn.1673-9450.2017.03.015

所属专题: 文献

综述

丁酸钠抗休克作用及机制研究进展
李琰光1, 刘锐2, 管秀红2, 戴跃龙3, 胡森4, 白晓东5,()   
  1. 1. 100039 北京,武警总医院烧伤整形科;121000 锦州医科大学研究生院
    2. 150036 哈尔滨,黑龙江省医院烧伤科
    3. 065000 廊坊,中国人民武装警察部队学院
    4. 100048 北京,解放军总医院第一附属医院烧伤研究所休克与多器官障碍实验室
    5. 100039 北京,武警总医院烧伤整形科
  • 收稿日期:2017-03-03 出版日期:2017-06-01
  • 通信作者: 白晓东
  • 基金资助:
    黑龙江省卫计委科研项目(2016-233); 黑龙江省科技厅青年自然基金(QC2016101)

Advances in research on anti - shock and mechanism of sodium butyrate

Yanguang Li1, Rui Liu2, Xiuhong Guan2, Yuelong Dai3, Sen Hu4, Xiaodong Bai5,()   

  1. 1. Department of Burn Surgery, the General Hospital of Armed Police Forces, Beijing 100039, China; Jinzhou Medical University Graduate School, Jinzhou 121000, China
    2. Department of Burn Surgery, Heilongjiang Provincial Hospital, Harbin 150036, China
    3. Chinese People′s Armed Police Force Academy, Langfang 065000, China
    4. Laboratory for Shock and Multiple Organ Dysfunction of Burns Institute, the First Affiliated Hospital of People′s Liberation Army General Hospital, Beijing 100048, China
    5. Department of Burn Surgery, the General Hospital of Armed Police Forces, Beijing 100039, China
  • Received:2017-03-03 Published:2017-06-01
  • Corresponding author: Xiaodong Bai
  • About author:
    Corresponding author: Bai Xiaodong, Email:
引用本文:

李琰光, 刘锐, 管秀红, 戴跃龙, 胡森, 白晓东. 丁酸钠抗休克作用及机制研究进展[J]. 中华损伤与修复杂志(电子版), 2017, 12(03): 223-227.

Yanguang Li, Rui Liu, Xiuhong Guan, Yuelong Dai, Sen Hu, Xiaodong Bai. Advances in research on anti - shock and mechanism of sodium butyrate[J]. Chinese Journal of Injury Repair and Wound Healing(Electronic Edition), 2017, 12(03): 223-227.

烧伤、创伤引起的急性血容量不足及大量渗出极易导致休克、多器官功能障碍甚至死亡,丁酸钠为I类非选择组蛋白去乙酰化酶抑制剂,近年研究表明丁酸钠不仅在抑制肿瘤细胞增殖、促进肿瘤细胞衰老和凋亡等方面起作用,在提高细胞对缺血、缺氧、炎症等打击的耐受能力方面同样有着积极的作用,丁酸钠保护休克后重要脏器的功能,其机制与诱导组蛋白过乙酰化、抑制核因子-κB和丝裂原活化蛋白激酶信号通路、保护血管内皮屏障有关,本文就近年关于丁酸钠抗创伤、烧伤休克及脓毒性休克的相关研究进展进行综述。

Burns, trauma caused by acute blood volume and a large number of exudation can easily lead to shock, multiple organ dysfunction or even death. Sodium butyrate is a class I non-selective histone deacetylase inhibitor. Recent studies have shown that sodium butyrate not only inhibits tumor cell proliferation, promotes tumor cell senescence and apoptosis, but also has a positive effect on improving the tolerance of cells to ischemia, hypoxia, inflammation and so on. Sodium butyrate can protect the vital organs after shock function. The mechanism is related to the induction of histone deacetylation, inhibition of nuclear factor-κB and mitogen-activated protein kinase signaling pathway, protection of vascular endothelium barrier, this paper on the recent sodium butyrate anti-trauma, burn shock and septic shock related research progress is summarized below.

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