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本文引用的文献

1
Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell Activation.丙泊酚通过抑制NADPH氧化酶介导的肥大细胞活化减轻小肠缺血再灌注损伤。
Oxid Med Cell Longev. 2015;2015:167014. doi: 10.1155/2015/167014. Epub 2015 Jul 12.
2
Propofol alleviates liver oxidative stress via activating Nrf2 pathway.丙泊酚通过激活Nrf2信号通路减轻肝脏氧化应激。
J Surg Res. 2015 Jun 15;196(2):373-81. doi: 10.1016/j.jss.2015.03.016. Epub 2015 Mar 19.
3
Potent anti-proliferative, pro-apoptotic activity of the Maytenus royleanus extract against prostate cancer cells: evidence in in-vitro and in-vivo models.罗伊卫矛提取物对前列腺癌细胞具有强大的抗增殖和促凋亡活性:体外和体内模型的证据
PLoS One. 2015 Mar 23;10(3):e0119859. doi: 10.1371/journal.pone.0119859. eCollection 2015.
4
The significance and mechanism of propofol on treatment of ischemia reperfusion induced lung injury in rats.丙泊酚对大鼠缺血再灌注诱导的肺损伤的治疗意义及机制
Cell Biochem Biophys. 2014 Dec;70(3):1527-32. doi: 10.1007/s12013-014-0088-0.
5
Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide.肝缺血再灌注损伤的机制及一氧化氮的保护作用。
World J Gastrointest Surg. 2014 Jul 27;6(7):122-8. doi: 10.4240/wjgs.v6.i7.122.
6
Propofol limits microglial activation after experimental brain trauma through inhibition of nicotinamide adenine dinucleotide phosphate oxidase.异丙酚通过抑制烟酰胺腺嘌呤二核苷酸磷酸氧化酶限制实验性颅脑损伤后的小胶质细胞激活。
Anesthesiology. 2013 Dec;119(6):1370-88. doi: 10.1097/ALN.0000000000000020.
7
Role of glycogen synthase kinase 3β in protective effect of propofol against hepatic ischemia-reperfusion injury.糖原合酶激酶 3β在丙泊酚减轻肝缺血再灌注损伤中的作用。
J Surg Res. 2013 Nov;185(1):388-98. doi: 10.1016/j.jss.2013.05.004. Epub 2013 May 24.
8
Role of heme oxygenase 1 in TNF/TNF receptor-mediated apoptosis after hepatic ischemia/reperfusion in rats.血红素加氧酶 1 在大鼠肝缺血/再灌注后 TNF/TNF 受体介导的细胞凋亡中的作用。
Shock. 2013 Apr;39(4):380-8. doi: 10.1097/SHK.0b013e31828aab7f.
9
Ischaemic preconditioning prevents the liver inflammatory response to lung ischaemia/reperfusion in a swine lung autotransplant model.缺血预处理可预防猪肺自体移植模型中肺缺血/再灌注引起的肝脏炎症反应。
Eur J Cardiothorac Surg. 2013 Jun;43(6):1194-201. doi: 10.1093/ejcts/ezs599. Epub 2012 Nov 23.
10
Pathogenic activity of circulating anti-desmoglein-3 autoantibodies isolated from pemphigus vulgaris patients.从寻常型天疱疮患者中分离出的循环抗桥粒芯糖蛋白 3 自身抗体的致病活性。
Arch Med Sci. 2012 May 9;8(2):347-56. doi: 10.5114/aoms.2012.28564.

丙泊酚预处理对人肝细胞缺血再灌注损伤的保护作用。

Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte.

作者信息

Zhang Yuzhu, Chen Zhenzhen, Feng Nianhai, Tang Junxia, Zhao Xingbo, Liu Chengxiao, Xu Hongyu, Zhang Mengyuan

机构信息

Department of Anesthesiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.

Department of Anesthesiology, Zibo Central Hospital, Zibo 255000, China.

出版信息

J Thorac Dis. 2017 Mar;9(3):702-710. doi: 10.21037/jtd.2017.02.80.

DOI:10.21037/jtd.2017.02.80
PMID:28449478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5394059/
Abstract

BACKGROUND

Blood reperfusion after ischemia is the main measure to restore cell function. This study was aimed to explore the effect of propofol on rat and cell models of liver ischemia-reperfusion (I/R) injury, and to investigate its possible mechanism.

METHODS

Wistar rats were divided into four groups: control group, sham group, I/R group, and propofol group. Human hepatocyte HL7702 was divided into six groups: control group, I/R group and propofol (5, 10, 20 and 40 µmol/L) groups. After the animal and cell models were established, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and adenosine triphosphate (ATP) levels in liver tissues and hepatocytes were measured. Cell viability and apoptosis of hepatocytes were respectively determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Furthermore, the expressions of apoptosis-related proteins in hepatocytes were determined by Western blot analysis.

RESULTS

ALT, AST and MDA levels were all decreased significantly, and the ATP level was increased significantly in propofol group compared with that in I/R group in both liver tissues and hepatocytes. Additionally, cell viability of hepatocytes in propofol group was higher than that in I/R group, while the percentage of apoptotic cells in propofol group was less than that in I/R group. Moreover, the expression of caspase-3 decreased and the expression of Bcl-2 increased significantly after propofol preconditioning.

CONCLUSIONS

Our findings suggested that propofol preconditioning might be an effective strategy for protecting the liver from I/R injury, which might provide a scientific basis for clinical application.

摘要

背景

缺血后血液再灌注是恢复细胞功能的主要措施。本研究旨在探讨丙泊酚对大鼠肝缺血再灌注(I/R)损伤模型及细胞模型的影响,并探究其可能的机制。

方法

将Wistar大鼠分为四组:对照组、假手术组、I/R组和丙泊酚组。将人肝细胞HL7702分为六组:对照组、I/R组以及丙泊酚(5、10、20和40 μmol/L)组。建立动物和细胞模型后,检测肝组织和肝细胞中的丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、丙二醛(MDA)和三磷酸腺苷(ATP)水平。分别采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐法和流式细胞术测定肝细胞活力和凋亡情况。此外,通过蛋白质印迹分析测定肝细胞中凋亡相关蛋白的表达。

结果

与I/R组相比,丙泊酚组肝组织和肝细胞中的ALT、AST和MDA水平均显著降低,ATP水平显著升高。此外,丙泊酚组肝细胞活力高于I/R组,而丙泊酚组凋亡细胞百分比低于I/R组。而且,丙泊酚预处理后caspase-3表达降低,Bcl-2表达显著增加。

结论

我们的研究结果表明,丙泊酚预处理可能是保护肝脏免受I/R损伤的有效策略,这可能为临床应用提供科学依据。