[1]董淑倩,李秋明,刘双珍.白血病抑制因子（LIF）对视网膜视锥细胞氧化损伤的保护作用及机制[J].眼科新进展,2017,37(6):506-510.[doi:10.13389/j.cnki.rao.2017.0128]
　DONG Shu-Qian,LI Qiu-Ming,LIU Shuang-Zhen.Protective effects and mechanisms of LIF on cone photoreceptors from oxidant injury[J].Recent Advances in Ophthalmology,2017,37(6):506-510.[doi:10.13389/j.cnki.rao.2017.0128]
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白血病抑制因子（LIF）对视网膜视锥细胞氧化损伤的保护作用及机制/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
37卷
期数:
2017年6期
页码:
506-510
栏目:
实验研究
出版日期:
2017-06-05

文章信息/Info

Title:
Protective effects and mechanisms of LIF on cone photoreceptors from oxidant injury
作者:
董淑倩; 李秋明; 刘双珍
450052　河南省郑州市，郑州大学第一附属医院眼科（董淑倩，李秋明）；410008　湖南省长沙市，中南大学湘雅医院眼科（董淑倩，刘双珍）
Author(s):
DONG Shu-Qian; LI Qiu-Ming; LIU Shuang-Zhen
Department of Ophthalmology，the First Affiliated Hospital of Zhengzhou University （DONG Shu-Qian，LI Qiu-Ming），Zhengzhou 450052，Henan Province，China；Department of Ophthalmology，Xiangya Hospital，Central South University（DONG Shu-Qian，LIU Shuang-Zhen），Changsha 410008，Hunan Province，China
关键词:
氧化损伤; 白血病抑制因子; 视锥细胞
Keywords:
oxidative injury; leukemia inhibitory factor; cone photoreceptor
分类号:
R774
DOI:
10.13389/j.cnki.rao.2017.0128
文献标志码:
A
摘要:
目的　研究氧化损伤条件下，白血病抑制因子（leukemia inhibitory factor，LIF）对视网膜视锥细胞活性的影响及其作用机制。方法　体外培养小鼠视网膜光感受器视锥细胞（661 W细胞株），根据干预药物不同，随机分为正常对照组、LIF干预组、H2O2干预组、S3I201干预组、H2O2+LIF干预组、H2O2+S3I201干预组、H2O2+LIF+ S3I201干预组。采用MTT比色法和Western blot法检测LIF预处理对氧化损伤后视锥细胞活性及其相关信号转导通路因子STAT3蛋白表达及其磷酸化水平的影响。运用S3I201阻断STAT3信号通路后，采用MTT比色法和实时荧光定量PCR检测STAT3信号通路阻断对氧化损伤后视锥细胞活性以及抗凋亡因子bcl-2和bcl-xl mRNA的表达影响。结果　与H2O2干预组相比，H2O2+LIF干预组p-Tyr705-STAT3蛋白的相对表达量明显增加，H2O2+S3I201干预组p-Tyr705-STAT3蛋白的相对表达量显著下降，差异均有统计学意义（均为P<0.05）。与H2O2干预组相比，H2O2+LIF干预组661 W细胞的细胞活性显著提高，差异有统计学意义（P<0.05）；与H2O2+LIF干预组相比，H2O2+LIF+ S3I201干预组661 W细胞的细胞活性显著下降，差异有统计学意义（P<0.05）。与正常对照组相比，LIF干预组、H2O2干预组和H2O2+LIF干预组bcl-2 mRNA和bcl-xl mRNA的相对表达量均显著增加，差异均有统计学意义（均为P<0.05）；与H2O2+LIF干预组相比，H2O2+LIF+S3I201干预组bcl-2 mRNA和bcl-xl mRNA的相对表达量均显著下降（均为P<0.05）。结论　LIF对视锥细胞氧化损伤具有保护作用，其可能通过激活STAT3信号通道刺激抑制凋亡因子bcl-2和bcl-xl的表达增加而发挥作用。
Abstract:
Objective　To investigate the role of leukemia inhibitory factor (LIF) in cell survival of cone photoreceptors and the underlying mechanism following oxidant injury.Methods　661W cells were cultured and randomly divided into normal control group，LIF intervention group，H2O2 intervention group，S3I201 intervention group，H2O2+LIF intervention group，H2O2+S3I201 intervention group and H2O2+LIF+S3I201 intervention group，according to the different intervention drugs.MTT assay and Western blot were used to detect the effects of LIF pretreatment on 661W activity and the expression of STAT3 protein and its phosphorylation level after oxidative damage.Using STAT3-specific inhibitor S3I201 to block the STAT3 signal transduction pathway，MTT assay and real-time PCR were used to detect the effects of STAT3 signaling pathway on 661W activity and the mRNA expression of survivin bcl-2 and bcl-xl after oxidative damage.Results　Compared to H2O2 intervention group，the relative protein expression of p-Tyr705-STAT3 was increased in H2O2+LIF intervention group，the difference was statistically significant (P<0.05)；The relative protein expression of p-Tyr705-STAT3 was decreased in H2O2+S3I201 intervention group，the difference was statistically significant (P<0.05).Compared to H2O2 intervention group，the cell activity of 661W cells was increased in H2O2+LIF intervention group，the difference was statistically significant(P<0.05).Compared to H2O2 +LIF intervention group，the cell activity of 661W cells was decreased in H2O2+LIF+ S3I201 intervention group，the difference was statistically significant (P<0.05).Compared to normal control group，the mRNA expression of bcl-2 and bcl-xl were increased in LIF intervention group，H2O2 intervention group and H2O2+LIF intervention group，the differences were statistically significant (all P<0.05).Compared to H2O2+LIF intervention group，the mRNA expression of bcl-2 and bcl-xl were decreased in H2O2+LIF+S3I201 intervention group，the differences were statistically significant (all P<0.05).Conclusion　LIF has protective effect on oxidative injury of cone photoreceptors，and it may contribute to cell survival through activation of the STAT3 signaling transduction pathway and its related survivin.

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备注/Memo

备注/Memo:
国家自然科学基金联合基金项目（编号：U1304812）；河南省医学科技攻关计划普通项目（编号：201602080）
更新日期/Last Update: 2017-06-28