[1]贾义,宋萍萍,周静,等.锌对3-吗啉-斯得酮亚胺（SIN-1）诱导的人晶状体上皮细胞Cu/Zn-SOD表达及活性的影响[J].眼科新进展,2017,37(1):024-27.[doi:10.13389/j.cnki.rao.2017.0006]
　JIA Yi,SONG Ping-Ping,ZHOU Jing,et al.Effects of zinc on expression and activity of Cu/Zn-SOD in human lens epithelial cells induced by SIN-1[J].Recent Advances in Ophthalmology,2017,37(1):024-27.[doi:10.13389/j.cnki.rao.2017.0006]
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锌对3-吗啉-斯得酮亚胺（SIN-1）诱导的人晶状体上皮细胞Cu/Zn-SOD表达及活性的影响/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
37卷
期数:
2017年1期
页码:
024-27
栏目:
实验研究
出版日期:
2017-01-05

文章信息/Info

Title:
Effects of zinc on expression and activity of Cu/Zn-SOD in human lens epithelial cells induced by SIN-1
作者:
贾义; 宋萍萍; 周静; 钟乃凤
550025　贵州省贵阳市，贵安新区大学城贵州医科大学生物与工程学院化学生物学教研室
Author(s):
JIA Yi; SONG Ping-Ping; ZHOU Jing; ZHONG Nai-Feng
Department of Chemical Biology，School of Biology and Engineering，Guizhou Medical University，Gui’an New District of Guiyang 550025，Guizhou Province，China
关键词:
人晶状体上皮细胞; 锌; 铜锌超氧化物歧化酶
Keywords:
human lens epithelial cells; zinc; Cu/Zn-SOD
分类号:
R776
DOI:
10.13389/j.cnki.rao.2017.0006
文献标志码:
A
摘要:
目的　研究补锌和缺锌条件下3-吗啉-斯得酮亚胺（SIN-1）对人晶状体上皮细胞铜锌超氧化物歧化酶（Cu/Zn-SOD）表达及活性的影响。方法　将培养的SRA01/04细胞系分为6组：对照组、SIN-1处理组、补锌组、补锌联合SIN-1处理组、缺锌组和缺锌联合SIN-1处理组。采用MTT法检测细胞存活率，Western blotting 和Cu/Zn-SOD活性检测试剂盒分别检测Cu/Zn-SOD蛋白表达和活性水平的变化。结果　我们选择对细胞存活率无显著影响的50 μmol·L-1 ZnSO4和1 μmol·L-1 N，N，N，N-四-(2-吡啶基甲基)乙二胺作为补锌和缺锌的条件，选择对细胞存活率有显著影响的500 μmol·L-1 SIN-1作为细胞受损的条件。在此条件下对照组、SIN-1处理组、补锌组、补锌联合SIN-1处理组、缺锌组和缺锌联合SIN-1处理组的细胞存活率分别为（100.0±1.4）%、（84.7±1.8）%、（101.2±1.6）%、（95.5±1.9）%、（100.9±2.3）%和（75.3±1.2）%，与对照组相比，SIN-1处理组和缺锌联合SIN-1处理组的细胞存活率均显著下降（均为P<0.05），与SIN-1处理组相比，补锌联合SIN-1处理组的细胞存活率显著升高（P<0.05），缺锌联合SIN-1处理组的细胞存活率则进一步下降（P<0.05）。各组的Cu/Zn-SOD蛋白相对表达量分别为1.005±0.007、0.991±0.015、1.044±0.008、0.945±0.007、1.278±0.011和0.850±0.057，Cu/Zn-SOD活性分别为(1.00±0.03)U、(0.85±0.05)U、(1.69±0.04)U、(1.35±0.05)U、(1.52±0.04)U和(1.09±0.03)U。与对照组相比，补锌组和缺锌组Cu/Zn-SOD蛋白表达量和活性均显著增加（均为P<0.05）。分别与补锌组或缺锌组相比，补锌联合SIN-1处理组和缺锌联合SIN-1处理组的Cu/Zn-SOD蛋白表达水平和活性均显著下降（均为P<0.05）。结论　补锌可以通过上调Cu/Zn-SOD的表达水平和活性，保护人晶状体上皮细胞抵抗由SIN-1造成的损伤，可能对白内障的形成有抑制作用。
Abstract:
Objective　To study the effects of zinc on the expression and activity of Cu/Zn-SOD in human lens epithelial cells (HLEC) induced by SIN-1.Methods　HLEC cell line SRA01/04 cells were cultured in DMEM medium and divided into six groups:control group,SIN-1 treatment group,zinc supplement group,zinc supplementation combined with SIN-1 treatment group,zinc deficiency group,zinc deficiency combined with SIN-1 treatment group.The cell viabilities were assayed by MTT,Cu/Zn-SOD protein levels and activities were detected by Western blotting and enzyme activity kit,respectively.Results　The cell viabilities of control group,SIN-1 treatment group,zinc supplement group,zinc supplementation combined with SIN-1 treatment group,zinc deficiency group,zinc deficiency combined with SIN-1 treatment group were (100.0±1.4)%,(84.7±1.8)%,(101.2±1.6)%,(95.5±1.9)%、(100.9±2.3)% and (75.3±1.2)%,respectively.The cell viabilities of zinc supplementation combined with SIN-1 treatment group were significantly increased,and those of zinc deficiency combined with SIN-1 treatment group were significantly decreased,compared with the SIN-1 treatment group (all P<0.05).The protein expressions of Cu/Zn-SOD in the six groups were 1.005±0.007,0.991±0.015,1.044±0.008,0.945±0.007,1.278±0.011 and 0.85±0.057,respectively.And the activities of Cu/Zn-SOD in the six groups were 1.00±0.03,0.85±0.05,1.69±0.04,1.35±0.05,1.52±0.04 and 1.09±0.03,respectively.The expression and activity of Cu/Zn-SOD were significantly increased in both zinc supplement group and deficiency group,compared with the control group (all P<0.05),and those of zinc supplementation combined with SIN-1 treatment group and zinc deficiency combined with SIN-1 treatment group were significantly decreased (all P<0.05),compared with the zinc supplement group or zinc deficiency group.Conclusion　Zinc can protect HLEC cells against SIN-1-induced cell damage through up-regulation of Cu/Zn-SOD expression levels and activity,thus may have a protective effect on the formation of cataract.

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备注/Memo

备注/Memo:
国家自然科学基金资助（编号：21561006）；贵州省科学技术基金资助（编号：黔科合J-2014-2028）；贵阳医学院博士启动基金（编号：YJ2014-8）
更新日期/Last Update: 2017-02-15