[1]王亚苹),张振坤),李 喆),等.重组人MG53蛋白激活Akt/GSK-3β通路降低LPS诱导的hUC-MSCs氧化损伤[J].郑州大学学报(医学版),2019,(04):522-526.[doi:10.13705/j.issn.1671-6825.2018.10.020]
 WANG Yaping),ZHANG Zhenkun),LI Zhe),et al.rhMG53 protein activates Akt/GSK-3β pathway to reduce LPS-induced oxidative damage to hUC-MSCs[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2019,(04):522-526.[doi:10.13705/j.issn.1671-6825.2018.10.020]
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重组人MG53蛋白激活Akt/GSK-3β通路降低LPS诱导的hUC-MSCs氧化损伤()
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《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2019年04期
页码:
522-526
栏目:
论著
出版日期:
2019-07-20

文章信息/Info

Title:
rhMG53 protein activates Akt/GSK-3β pathway to reduce LPS-induced oxidative damage to hUC-MSCs
作者:
王亚苹1)张振坤1)李 喆1)刘腾飞1)黄团结1)周馨魁1) 麻建杰2)关方霞1)马珊珊1)
1)郑州大学生命科学学院 郑州450001;2)美国俄亥俄州立大学戴维斯心肺研究所 哥伦布市 43210
Author(s):
WANG Yaping1) ZHANG Zhenkun1) LI Zhe1) LIU Tengfei1) HUANG Tuanjie1) ZHOU Xinkui1) MA Jianjie2) GUAN Fangxia1) MA Shanshan1)
1)College of Life Sciences, Zhengzhou University, Zhengzhou 450001;2)Davis Heart and Lung Research Institute, the Ohio State University, Columbus, OH, 43210 USA
关键词:
重组人MG53 脂多糖 脐带间充质干细胞 氧化损伤
Keywords:
rhMG53 lipopolysaccharide hUC-MSC oxidative damage
分类号:
Q28
DOI:
10.13705/j.issn.1671-6825.2018.10.020
摘要:
目的:探讨重组人MG53蛋白对人脐带间充质干细胞(hUC-MSCs)氧化损伤的保护作用及分子机制。方法:实验分为对照组(CON组,不处理)、LPS组(加入200 mg/L LPS)、MG53组(加入30 mg/L重组人MG53蛋白)和MG53+LPS组(同时加入重组人MG53蛋白和LPS),48 h 后,采用CCK-8法检测细胞活力,AO-EB染色检测细胞凋亡,JC-1染色评价线粒体膜电位变化,DCFH-DA荧光探针法检测细胞内活性氧(ROS)水平,酶标法检测丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和过氧化氢酶(CAT)活性,Western blot法检测磷酸化Akt和GSK-3β蛋白的表达。结果:与LPS组相比,MG53+LPS组细胞存活率升高,凋亡率和线粒体膜电位降低,细胞内ROS和MDA含量降低, SOD和CAT活性升高,同时磷酸化Akt和磷酸化GSK-3β的表达升高(P<0.05)。结论:重组人MG53蛋白可能通过激活Akt/GSK-3β信号通路,保护hUC-MSCs免受LPS诱导的氧化损伤。
Abstract:
Aim:To investigate the protective effects of rhMG53 protein on LPS-induced oxidative damage to human umbilical cord mesenchymal stem cells(hUC-MSCs).Methods:hUC-MSCs were divided into control group(CON group), LPS group(200 mg/L LPS), MG53 group(30 mg/L rhMG53),and MG53+LPS group.After 48 hours,cell viability was detected by CCK-8 assay, apoptosis was detected by AO-EB staining, mitochondrial membrane potential was measured by JC-1 staining, intracellular reactive oxygen species(ROS)level was detected by DCFH-DA fluorescence probing method, malondialdehyde(MDA)content, and superoxide dismutase(SOD)and catalase(CAT)activity were detected by enzyme labeling method,and Western blot was used to analyze the expressions of phosphorylated Akt and GSK-3β.Results:Compared with LPS group, the viability rate in MG53+LPS group increased, apoptosis rate and mitochondrial membrane potential decreased,ROS production and MDA content were lower, and SOD and CAT activities were higher(P<0.05). In addition, the expressions of LPS-induced phosphorylated Akt and phosphorylated GSK-3β also increased in MG53+LPS group(P<0.05).Conclusion:rhMG53 could protect hUC-MSCs from LPS-induced oxidative damage by activating the Akt/GSK-3β signaling pathway.

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备注/Memo

备注/Memo:
【基金项目】国家自然科学基金资助项目(81601078,81471306); 河南省高校科技创新团队项目(15IRTSTHN022); 河南省重点科技攻关项目(152102310272)
【作者简介】马珊珊,通信作者,女,1984年5月生,博士,副教授,研究方向:生物医学,E-mail:mashanshan84@163.com; 关方霞,通信作者,女,1969年2月生,博士,教授,研究方向:干细胞与生物医学,E-mail:guanfangxia@126.com
更新日期/Last Update: 2019-07-20