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[1]吕景淑,贾莉莉,喻文立.异丙酚通过诱导幼鼠海马神经元线粒体自噬减轻其肝缺血再灌注后脑损伤[J].天津医科大学学报,2019,25(01):28-31.
 LV Jing-shu,JIA Li-li,YU Wen-li.Propofol alleviated brain damage by inducing mitophagy in hippocampal neurons after hepatic ischemia and reperfusion in young mice[J].Journal of Tianjin Medical University,2019,25(01):28-31.
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异丙酚通过诱导幼鼠海马神经元线粒体自噬减轻其肝缺血再灌注后脑损伤(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
25卷
期数:
2019年01期
页码:
28-31
栏目:
基础医学
出版日期:
2019-01-20

文章信息/Info

Title:
Propofol alleviated brain damage by inducing mitophagy in hippocampal neurons after hepatic ischemia and reperfusion in young mice
文章编号:
1006-8147(2019)01-0028-04
作者:
吕景淑1贾莉莉2喻文立2
(1.天津医科大学一中心临床学院麻醉科,天津300192;2.天津市第一中心医院麻醉科,天津300192)
Author(s):
LV Jing-shu1 JIA Li-li2 YU Wen-li2
(1. Department of Anesthesiology, First Center Clinical College, Tianjin Medical Hospital,Tianjin 300192 China; 2. Department of Anesthesiology, Tianjin First Central Hospital, Tianjin 300192, China)
关键词:
异丙酚肝缺血再灌注海马神经元线粒体自噬
Keywords:
spropofol hepatic ischemia and perfusion hippocampal neurons mitophagy
分类号:
R614
DOI:
-
文献标志码:
A
摘要:
目的:探究异丙酚对肝缺血再灌注后幼鼠海马神经元线粒体自噬的影响。方法: C57BL/6两周龄的小鼠40只被随机分成4组(n=10):假手术组(S组),肝缺血再灌注组(IR组),异丙酚组(P组),异丙酚+自噬抑制剂3-MA组(3-MA组),除S组仅进行开关腹操作外,其余各组均行缺血60 min,再灌注6h建模。取血组织标本及海马组织标本。ELISA法检测血清中脑损伤标志物神经元特异性烯醇化酶(NSE)和S100β浓度及炎症因子白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)的浓度;透射电镜法观察自噬小体和线粒体超微结构;Western blot法检测自噬相关蛋白LC3Ⅱ、Nix及凋亡蛋白Caspase-3的表达水平。结果:(1)脑损伤标志物和炎症因子水平, 3-MA组最高,其次为IR组,P组居中,S组最低(P<0.05);(2)自噬小体,P组最多,且线粒体结构较完整,依次为IR和S组,3-MA组自噬最少,线粒体肿胀,分裂最多;(3)LC3Ⅱ、Nix蛋白表达水平同上述线粒体自噬水平一致,Caspase-3与此相反(P<0.05)。结论:异丙酚可促进肝缺血再灌注后幼鼠海马神经元的线粒体自噬,减轻炎症反应,减少细胞凋亡。
Abstract:
Objective: To explore the effects of propofol on hippocampal neurons mitophagy after hepatic ischemia and reperfusion in young mice. Methods: Two-week old C57BL/6 mice were randomly divided into 4 groups (n=10): sham operation group (group S); hepatic ischemia-reperfusion group (group M); propofol group (group P); propofol+ 3-MA group (group 3-MA). Besides the sham group that only had abdominal open and close operations, the rest of the groups underwent 60min ischemia and reperfusion for 6h. Blood samples and brain tissues were collected. ELISA was used to detect brain injury markers: neuron specific enolase (NSE) , S100β and inflammatory factors: interleukin-6 ( IL-6 ) , tumor necrosis factor-alpha ( TNF -α ); transmission electron microscope (TEM) was used to observe the structure of autophagosome and mitochondria; protein LC3 II, Nix, caspase-3 expression levels were assessed by Western blot. Results:(1) Concentrations of brain injury markers and inflammatory factors were highest in group 3-MA, followed by group IR, group P, and group sham (P<0.05); (2) the number of autophagosome was biggest in group P, followed by group IR, group S and group 3-MA; mitochondria structure was relatively unbroken in group S, followed by group P, group IR and group 3-MA; (3) LC3 II and Nix protein expression levels were consistent with TEM results, while caspase-3 was opposite(P<0.05). Conclusion: Propofol can promote hippocampal neurons mitophagy after hepatic ischemia and reperfusion in young mice, and reduce inflammation and cell apoptosis.

参考文献/References:


[1] Yazigi N A. Long term outcomes after pediatric liver transplantation[J]. Pediatr Gastroenterol Hepatol Nutr, 2013,16(4):207
[2] Wan P, Xu D, Zhang J, et al. Liver transplantation for biliary atresia: A nationwide investigation from 1996 to 2013 in mainland China[J]. Pediatr Transplant, 2016,20(8):1051
[3] Bernhardt M, Pflugrad H, Goldbecker A, et al. Central nervous system complications after liver transplantation: common but mostly transient phenomena[J]. Liver Transpl, 2015,21(2):224
[4] Nastos C, Kalimeris K, Papoutsidakis N, et al. Global consequences of liver ischemia/reperfusion injury[J]. Oxid Med Cell Longev, 2014,2014:906965
[5] Wang W, Lu R, Feng D Y, et al. Inhibition of microglial activation contributes to propofol-induced protection against post-cardiac arrest brain injury in rats[J]. J Neurochem, 2015,134(5):892
[6] Wang L, Tang W, Jiang T, et al. Endoplasmic reticulum stress is involved in the neuroprotective effect of propofol[J]. Neurochem Res, 2014,39(9):1741
[7] Nakajima A, Tsuji M, Inagaki M, et al. Neuroprotective effects of propofol on ER stress-mediated apoptosis in neuroblastoma SH-SY5Y cells[J]. Eur J Pharmacol, 2014,725:47
[8] Shi S S, Yang W Z, Chen Y, et al. Propofol reduces inflammatory reaction and ischemic brain damage in cerebral ischemia in rats[J]. Neurochem Res, 2014,39(5):793
[9] 麻勇, 汪大伟, 刘连新, 等. 小鼠肝脏部分缺血再灌注损伤模型的建立[J]. 中华消化外科杂志, 2013,12(9):703
[10] Zhang J, Randall M S, Loyd M R, et al. Mitochondrial clearance is regulated by Atg7-dependent and -independent mechanisms during reticulocyte maturation[J]. Blood, 2009,114(1):157
[11] Wu H, Chen Q. Hypoxia activation of mitophagy and its role in disease pathogenesis[J]. Antioxid Redox Signal, 2015,22(12):1032
[12] Qin J, Zhou J, Dai X, et al. Short-term starvation attenuates liver ischemia-reperfusion injury (IRI) by Sirt1-autophagy signaling in mice[J]. Am J Transl Res, 2016,8(8):3364
[13] Ding S, Jiang J, Zhang G, et al. Resveratrol and caloric restriction prevent hepatic steatosis by regulating SIRT1-autophagy pathway and alleviating endoplasmic reticulum stress in high-fat diet-fed rats[J]. PLoS One, 2017,12(8):e183541
[14] 宋虎, 张建军, 王振, 等. FOXO3a调控线粒体自噬在肝脏缺血再灌注损伤中的作用[J]. 天津医药, 2017(12):1242
[15] Kim E J, Choi I S, Yoon J Y, et al. Effects of propofol-induced autophagy against oxidative stress in human osteoblasts[J]. J Dent Anesth Pain Med, 2016,16(1):39
[16] Chang C Y, Chen P H, Lu S C, et al. Propofol-enhanced autophagy increases motility and angiogenic capacity of cultured human umbilical vascular endothelial cells[J]. Life Sci, 2015,142:49
[17] Li H, Zhang X, Tan J, et al. Propofol postconditioning protects H9c2 cells from hypoxia/reoxygenation injury by inducing autophagy via the SAPK/JNK pathway[J]. Mol Med Rep, 2018,17(3):4573
[18] Yoon J Y, Jeon H O, Kim E J, et al. Propofol protects human keratinocytes from oxidative stress via autophagy expression[J]. J Dent Anesth Pain Med, 2017,17(1):21
[19] Yoon J Y, Baek C W, Kim E J, et al. Propofol protects against oxidative-stress-induced COS-7 cell apoptosis by inducing autophagy[J]. J Dent Anesth Pain Med, 2017,17(1):37
[20] Cui D R, Wang L, Jiang W, et al. Propofol prevents cerebral ischemia-triggered autophagy activation and cell death in the rat hippocampus through the NF-kappaB/p53 signaling pathway[J]. Neuroscience, 2013,246:117
[21] Li P, Hao X C, Luo J, et al. Propofol Mitigates Learning and Memory Impairment After Electroconvulsive Shock in Depressed Rats by Inhibiting Autophagy in the Hippocampus[J]. Med Sci Monit, 2016,22:1702
[22] Chen X, Li K, Zhao G. Propofol Inhibits HeLa Cells by Impairing Autophagic Flux via AMP-Activated Protein Kinase (AMPK) Activation and Endoplasmic Reticulum Stress Regulated by Calcium[J]. Med Sci Monit, 2018,24:2339
[23] Yang N, Li L, Li Z, et al. Protective effect of dapsone on cognitive impairment induced by propofol involves hippocampal autophagy[J]. Neurosci Lett, 2017,649:85

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备注/Memo

备注/Memo:
基金项目 天津市卫生行业重点攻关项目(16KG101);天津市卫生和计划生育委员会中医中西医结合科研课题(2017056);天津市自然科学基金面上项目(17JCYBJC28000);2017年天津医学会麻醉学分会中青年科研培育基金项目(TJMZJJ-2017-01)
作者简介 吕景淑(1994-),女,硕士在读,研究方向:肝缺血再灌注后的脑损伤;通信作者:喻文立, E-mail:yzxyuwenli@163.com。
更新日期/Last Update: 2019-03-01