切换至 "中华医学电子期刊资源库"

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/OL]. 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/OL]. 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.

1
Fessler EB,Chibane FL,Wang Z, et al. Potential roles of HDAC inhibitors in mitigating ischemia-induced brain damage and facilitating endogenous regeneration and recovery[J]. Curr Pharm Des, 2013, 19(28): 5105-5120.
2
Wu G,Nan C,Rollo JC, et al. Sodium valproate-induced congenital cardiac abnormalities in mice are associated with the inhibition of histone deacetylase[J]. J Biomed Sci, 2010, 17: 16.
3
Gonzales ER,Chen H,Munuve RM, et al. Hepatoprotection and lethality rescue by histone deacetylase inhibitor valproic acid in fatal hemorrhagic shock[J]. J Trauma, 2008, 65(3): 554-565.
4
Imanishi R,Ohtsuru A,Iwamatsu M, et al. A histone deacetylase inhibitor enhances killing of undifferentiated thyroid carcinoma cells by p53 gene therapy[J]. J Clin Endocrinol Metab, 2002, 87(10): 4821-4924.
5
Takai N,Desmond JC,Kumagai T, et al. Histone deacetylase inhibitors have a profound antigrowth activity in endometrial cancer cells[J]. Clin Cancer Res, 2004, 10(3):1141-1149.
6
Faraco G,Pancani T,Formentini L, et al. Pharmacological inhibition of histone deacetylases by suberoylanilide hydroxamic acid specifically alters gene expression and reduces ischemic injury in the mouse brain[J]. Mol Pharmacol, 2006, 70(6): 1876-1884.
7
Li Y,Yuan Z,Liu B, et al. Prevention of hypoxia-Induced neuronal apoptosis through histone deacetylase inhibition [J]. J Trauma, 2008, 64(4): 863-870.
8
唐富波,何波,张文华, 等. 丁酸钠对严重烫伤后大鼠肝脏血流量及水肿的影响[J]. 中国现代医学杂志, 2016, 26(5): 7-10.
9
Candido EP,Reeves R,Davie JR. Sodium butyrate inhibits histone deacetylation in cultured cells[J]. Cell, 1978, 14(1): 105-113.
10
Li Y,Alam HB. Creating a pro-survival and anti-inflammatory phenotype by modulation of acetylation in models of hemorrhagic and septic shock[J]. Adv Exp Med Biol, 2012, 710: 107-133.
11
Liang X,Wang RS,Wang F, et al. Sodium butyrate protects against severe burn-induced remote acute lung injury in rats[J]. PLoS One, 2013, 8(7): e68786.
12
Zacharias N,Sailhamer EA,Li Y, et al. Histone deacetylase inhibitors prevent apoptosis following lethal hemorrhagic shock in rodent kidney cells[J]. Resuscitation, 2011, 82(1): 105-109.
13
Ma X,Fan PX,Li LS, et al. Butyrate promotes the recovering of intestinal wound healing through its positive effect on the tight junctions[J]. J Anim Sci, 2012, 90 Suppl 4: 266-268.
14
Hu X,Zhang K,Xu C, et al. Anti-inflammatory effect of sodium butyrate preconditioning during myocardial ischemia/reperfusion[J]. Exp Ther Med, 2014, 8(1): 229-232.
15
唐富波,张文华,李雨梦, 等. 丁酸钠对特重度烧伤大鼠脏器功能及血流量的影响[J/CD]. 中华损伤与修复杂志(电子版), 2016, 11(2): 90-95.
16
Sun J,Wang F,Li H, et al. Neuroprotective effect of sodium butyrate against cerebral ischemia/reperfusion injury in mice[J]. Biomed Res Int, 2015, 2015: 395895.
17
Finkelstein RA,Li Y,Liu B, et al. Treatment with histone deacetylase inhibitor attenuates MAP kinase mediated liver injury in a lethal model of septic shock[J]. J Surg Res, 2010, 163(1): 146-154.
18
Kiernan R,Brès V,Ng RW, et al. Post-activation turn-off of NF-kappa B-dependent transcription is regulated by acetylation of p65[J]. J Biol Chem, 2003, 278(4): 2758-2766.
19
Inan MS,Rasoulpour RJ,Yin L. The luminal short-chain fatty acid butyrate modulates NF-κB activity in a human colonic epithelial cell line[J]. Gastroenterology, 2000, 118(4): 724-734.
20
Cao W,Bao C,Padalko E, et al. Acetylation of mitogen-activated protein kinase phosphatase-1 inhibits toll-like receptor signaling[J]. J Exp Med, 2008, 205(6): 1491-1503.
21
王君,朱光发. 脓毒症与核因子-κB信号通路关系的研究进展[J]. 感染、炎症、修复, 2011, 12(2): 121-123.
22
Chakravortty D,Koide N,Kato Y, et al. The inhibitory action of butyrate on lipopolysaccharide-induced nitric oxide production in RAW 264.7 murine macrophage cells[J]. J Endotoxin Res, 2000, 6(3): 243-247.
23
Yoo SY,Chung C,Kim JK, et al. Perinuclear translocation of hsp 27 in shear stress exposed human endothelial cells[J]. Biotechnol Lett, 2005, 27(6): 443-448.
24
Chan JY,Wang SH,Chan SH. Differential roles of iNOS and nNOS at rostral ventrolateral medulla during experimental endotoxemia in the rat[J]. Shock, 2001, 15(1): 65-72.
25
Sprung CL,Annane D,Keh D, et al. Hydrocortisone therapy for patients with septic shock[J]. N Engl J Med, 2008, 358(2): 111-124.
26
Hayden MS,Ghosh S. Shared Principles in NF-κB Signaling[J]. Cell, 2008, 132(3): 344-362.
27
Zhang LT,Yao YM,Lu JQ, et al. Sodium butyrate prevents lethality of severe sepsis in rats[J]. Shock, 2007, 27(6): 672-677.
28
Kim HJ,Rowe M,Ren M, et al. Histone deacetylase inhibitors exhibit anti-inflammatory and neuroprotective effects in a rat permanent ischemic model of stroke: multiple mechanisms of action[J]. J Pharmacol Exp Ther, 2007, 321(3): 892-901.
29
Hu X,Zhang K,Xu C, et al. Anti-inflammatory effect of sodium butyrate preconditioning during myocardial ischemia/reperfusion[J]. Exp Ther Med, 2014, 8(1): 229-232.
30
Feng Y,Yang Q,Xu J, et al. Effects of HMGB1 on PMN apoptosis during LPS-induced acute lung injury[J]. Exp Mol Pathol, 2008, 85(3): 214-222.
31
Gong Q,Zhang H,Li JH, et al. High-mobility group box 1 exacerbates concanavalin A-induced hepatic injury in mice[J]. J Mol Med(Berl), 2010, 88(12):1289-1298.
32
Naglova H,Bucova M. HMGB1 and its physiological and pathological roles[M]. Bratisl Lek Listy, 2012, 113(3): 163-171.
33
Romero R,Chaiworapongsa T,Alpay Savasan Z, et al. Damage-associated molecular patterns (DAMPs) in preterm labor with intact membranes and preterm PROM: a study of the alarmin HMGB1[J]. J Matern Fetal Neonatal Med, 2011, 24(12): 1444-1455.
34
Abraham E,Arcaroli J,Carmody A, et al. HMG-1 as a mediator of acute lung inflammation[J]. J Immunol, 2000, 165(6): 2950-2954.
35
Lutz W,Stetkiewicz J. High mobility group box 1 protein as a late-acting mediator of acute lung inflammation[J]. Int J Occup Med Environ Health, 2004, 17(2): 245-254.
36
Ueno H,Matsuda T,Hashimoto S, et al. Contributions of high mobility group box protein in experimental and clinical acute lung injury[J]. Am J Respir Crit Care Med, 2004, 170(12): 1310-1316.
37
Bitto A,Barone M,David A, et al. High mobility group box-1 expression correlates with poor outcome in lung injury patients[J]. Pharmacol Res, 2010, 61(2): 116-120.
38
董宁,姚咏明,黄显金, 等. 严重烧伤患者CD14基因多态性对高迁移率族蛋白B1表达的影响[J]. 中华烧伤杂志, 2010, 26(2): 109-112.
39
Costantini TW,Loomis WH,Putnam JG, et al. Burn-induced gut barrier injury is attenuated by phosphodiesterase inhibition:effects on tight junction structural proteins[J]. Shock, 2009, 31(4): 416-422.
40
Krzyzaniak M,Cheadle G,Peterson C, et al. Burn-induced acute lung injury requires a functional Toll-like receptor 4[J]. Shock, 2011, 36(1): 24-29.
41
Fang Y,Xu P,Gu C, et al. Ulinastatin improves pulmonary function in severe burn-induced acute lung injury by attenuating inflammatory response[J]. J Trauma, 2011, 71(5): 1297-1304.
42
Dejana E. Endothelial cell-cell junctions: happy together[J]. Nat Rev Mol Cell Biol, 2004, 5(4): 261-270.
43
张家平,黄跃生,汪仕良. 烧伤后早期血管通透性增高研究进展[J]. 中华烧伤杂志, 2010, 26(5): 343-346.
44
Steed E,Balda MS,Matter K. Dynamics and functions of tight junctions[J]. Trends Cell Biol, 2010, 20(3): 142-149.
45
Han X,Song H,Wang Y, et al. Sodium butyrate protects the intestinal barrier function in peritonitic mice[J]. Int J Clin Exp Med, 2015, 8(3): 4000-4007.
46
Wang HB,Wang PY,Wang X, et al. Butyrate enhances intestinal epithelial barrier function via up-regulation of tight junction protein Claudin-1 transcription[J]. Dig Dis Sci, 2012, 57(12): 3126-3135.
47
Saito S,Lasky JA,Guo W, et al. Pharmacological inhibition of HDAC6 attenuates endothelial barrier dysfunction induced by thrombin[J]. Biochem Biophys Res Commun, 2011, 408(4): 630-634.
48
唐富波,郭静,郑金光, 等. 丁酸钠对严重烫伤大鼠肾血流量和微血管通透性的影响[J]. 武警医学, 2016, 27(1): 8-11.
49
Kim DJ,Martinez-Lemus LA,Davis GE. EB1, p150Glued, and Clasp1 control endothelial tubulogenesis through microtubule assembly, acetylation, and apical polarization[J]. Blood, 2013, 121(17): 3521-3530.
[1] 王晓亚, 王燕芸, 顾永忠. 产科快速反应团队成功救治心脏骤停孕产妇1例并文献复习[J/OL]. 中华妇幼临床医学杂志(电子版), 2024, 20(02): 148-156.
[2] 徐保平, 彭怀文, 喻怀斌, 王晓涛. 新型冠状病毒肺炎继发糖尿病酮症酸中毒合并肝门静脉积气一例[J/OL]. 中华实验和临床感染病杂志(电子版), 2024, 18(04): 250-255.
[3] 周润奭, 郑敏, 韩伟, 李尊柱, 何朝凯, 池熠, 隆云. 目标导向的集束化护理策略对多重耐药菌所致感染性休克患者28 d预后的影响[J/OL]. 中华重症医学电子杂志, 2024, 10(03): 236-242.
[4] 庞明敏, 闫美辰, 刘光凤, 宫继斌, 许娜娜, 郑玥, 范少华, 王昊. 脓毒症液体复苏治疗策略的研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(02): 189-195.
[5] 杨磊, 汪美华, 胡锦. 急性脑梗死去骨瓣术后合并碳青霉烯耐药肺炎克雷伯菌感染一例[J/OL]. 中华重症医学电子杂志, 2024, 10(02): 200-204.
[6] 李莉, 张丽娜, 钱招昕. 亚甲蓝——脓毒症休克的“魔法锦囊”?[J/OL]. 中华重症医学电子杂志, 2024, 10(02): 136-142.
[7] 张引, 李国强. 亚甲蓝治疗脓毒症休克的研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(02): 143-147.
[8] 董晟, 郎胜坤, 葛新, 孙少君, 薛明宇. 反向休克指数乘以格拉斯哥昏迷评分对老年严重创伤患者发生急性创伤性凝血功能障碍的预测价值[J/OL]. 中华临床医师杂志(电子版), 2024, 18(06): 541-547.
[9] 宫平, 刘倩, 王啸, 袁会敏, 王维展, 王璞. 早期PI联合Pv-aCO2/Ca-vO2预测老年脓毒性休克的死亡风险[J/OL]. 中华临床医师杂志(电子版), 2024, 18(03): 253-258.
[10] 刘亮, 肖浩, 崔晓磊, 吕宝谱, 张睿, 郑拓康, 孟庆冰, 姚冬奇, 田英平, 高恒波. 急性心肌梗死合并心源性休克患者预后因素分析97例[J/OL]. 中华临床医师杂志(电子版), 2024, 18(02): 183-189.
[11] 傅新露, 李之岳, 卢丹. 妊娠合并结肠癌穿孔致脓毒症休克一例并文献复习[J/OL]. 中华产科急救电子杂志, 2024, 13(04): 227-231.
[12] 胡琴, 莫伟, 中国研究型医院学会出血专业委员会, 中国出血中心联盟护理专家委员会. 失血性休克急救护理专家共识[J/OL]. 中华介入放射学电子杂志, 2024, 12(03): 193-199.
[13] 轩欢欢, 刘凤麟, 李伟, 李自普, 贾宝俊, 王金菊, 满宜刚. 儿童川崎病休克综合征合并可逆性胼胝体压部病变综合征的诊断学特征并文献复习[J/OL]. 中华诊断学电子杂志, 2024, 12(02): 95-100.
[14] 龚霄雷, 朱丽敏, 姜燕, 徐卓明. 急性右心室功能障碍的诊疗进展[J/OL]. 中华心脏与心律电子杂志, 2024, 12(03): 161-168.
[15] 詹维强, 李梦蝶, 涂玉玲, 郭艳, 芦乙滨, 史新格, 许明. 早期CRRT联合VA-ECMO治疗难治性心源性休克的临床效果[J/OL]. 中华卫生应急电子杂志, 2024, 10(05): 260-268.
阅读次数
全文


摘要


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?