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CLC number: Q291

On-line Access: 2018-06-04

Received: 2017-05-27

Revision Accepted: 2017-07-12

Crosschecked: 2018-05-14

Cited: 0

Clicked: 3170

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Kai-qiang Li

https://orcid.org/0000-0003-4307-0845

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Journal of Zhejiang University SCIENCE B 2018 Vol.19 No.6 P.436-444

http://doi.org/10.1631/jzus.B1700277


Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice


Author(s):  Bing-yu Chen, Lu-xi Jiang, Ke Hao, Lu Wang, Ying Wang, Yi-wei Xie, Jian Shen, Meng-hua Zhu, Xiang-ming Tong, Kai-qiang Li, Zhen Wang

Affiliation(s):  Research Center of Blood Transfusion Medicine, Ministry of Education Key Laboratory of Laboratory Medicine, Department of Blood Transfusion, Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou 310014, China; more

Corresponding email(s):   lkq252526@163.com, zhenwangzjpph@163.com

Key Words:  Fulminant hepatic failure, Plasma, Inflammation, Apoptosis


Bing-yu Chen, Lu-xi Jiang, Ke Hao, Lu Wang, Ying Wang, Yi-wei Xie, Jian Shen, Meng-hua Zhu, Xiang-ming Tong, Kai-qiang Li, Zhen Wang. Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice[J]. Journal of Zhejiang University Science B, 2018, 19(6): 436-444.

@article{title="Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice",
author="Bing-yu Chen, Lu-xi Jiang, Ke Hao, Lu Wang, Ying Wang, Yi-wei Xie, Jian Shen, Meng-hua Zhu, Xiang-ming Tong, Kai-qiang Li, Zhen Wang",
journal="Journal of Zhejiang University Science B",
volume="19",
number="6",
pages="436-444",
year="2018",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1700277"
}

%0 Journal Article
%T Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice
%A Bing-yu Chen
%A Lu-xi Jiang
%A Ke Hao
%A Lu Wang
%A Ying Wang
%A Yi-wei Xie
%A Jian Shen
%A Meng-hua Zhu
%A Xiang-ming Tong
%A Kai-qiang Li
%A Zhen Wang
%J Journal of Zhejiang University SCIENCE B
%V 19
%N 6
%P 436-444
%@ 1673-1581
%D 2018
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1700277

TY - JOUR
T1 - Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice
A1 - Bing-yu Chen
A1 - Lu-xi Jiang
A1 - Ke Hao
A1 - Lu Wang
A1 - Ying Wang
A1 - Yi-wei Xie
A1 - Jian Shen
A1 - Meng-hua Zhu
A1 - Xiang-ming Tong
A1 - Kai-qiang Li
A1 - Zhen Wang
J0 - Journal of Zhejiang University Science B
VL - 19
IS - 6
SP - 436
EP - 444
%@ 1673-1581
Y1 - 2018
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1700277


Abstract: 
fulminant hepatic failure is a severe clinical condition associated with extremely poor outcomes and high mortality. A number of studies have demonstrated the ability of plasma transfusion to successfully treat fulminant hepatic failure, but the underlying mechanisms are not well understood. The aim of the present study is to define the mechanisms of plasma transfusion treatment in lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced mice. LPS/D-GalN treatment in mice causes significant hepatic failure, including increasing serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, histopathological changes in centrilobular necrosis and inflammatory cells, and the up-regulation of inflammation (tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)). When LPS/D-GaIN-induced mice were treated with plasma, these changes were halted. Results showed that plasma transfusion significantly reduced mortality, and decreased the levels of AST, ALT, and inflammation factors such as TNF-α and IL-6. The expression levels of cleaved Caspase-3, BAX, and p53 were down-regulated and Bcl-2 was up-regulated, suggesting that plasma can reduce LPS/D-GalN-induced apoptosis. The protective mechanism of plasma against LPS/D-GalN-induced fulminant hepatic failure is related to the inhibition of the inflammatory response and the reduction in apoptosis through the down-regulation of the p53-induced apoptotic pathway.

血浆输注通过抑制肝细胞凋亡对脂多糖/D-半乳糖诱导的小鼠急性肝损伤的保护作用

目的:评估血浆输注对脂多糖/D-半乳糖(LPS/D-GalN)诱导的小鼠急性肝损伤的保护作用,并探讨其作用机制.
创新点:在小鼠急性肝损伤模型中证明血浆输注对肝损伤的保护作用,且此作用与p53介导的肝细胞凋亡相关.
方法:将40只清洁型ICR雄性小鼠随机分为4组 (n=10每组):(1)对照组;(2)血浆(plamsa)组;(3)LPS/D-GalN组;(4)LPS/D-GalN+plamsa组.收集血清和肝组织样本,用天门冬氨酸转氨酶(AST)和丙氨酸氨基转移酶(ALT)试剂盒检测血清中AST和ALT水平;用酶联免疫吸附法(ELISA)检测肝组织中白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达变化;肝组织进行苏木精-伊红染色法(HE)和网状纤维染色,显微镜下观察肝组织病理学变化;用免疫印迹法(WB)检测凋亡相关蛋白的变化.在腹腔注射LPS/D-GalN后 32小时内对小鼠进行存活分析.
结论:LPS/D-GalN能够显著诱导小鼠的急性肝损伤,包括增加血清中AST和ALT水平;中心小叶坏死和炎性细胞的组织病理学变化和炎症上调(TNF-α和IL-6).当血浆输注后,这些变化被缓解.结果显示,血浆输注显著降低小鼠死亡率,降低AST、ALT和炎症因子如TNF-α和IL-6的水平.Cleaved Caspase-3、BAX和p53的表达下调,Bcl-2上调,表明血浆可以减少LPS/D-GalN诱导的细胞凋亡.血浆输注对LPS/D-GalN诱导的急性肝损伤的保护机制与通过p53诱导的凋亡途径和炎症因子减少相关.

关键词:肝损伤;血浆;炎症;凋亡

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

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