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JNK1/2信号通路在砷致细胞凋亡中双向效应的Meta分析
引用本文:胡云华,王仁举,张子怡,孙立明,丁玉松,芮东升,牛强,宋关玲,郭淑霞,李述刚.JNK1/2信号通路在砷致细胞凋亡中双向效应的Meta分析[J].现代预防医学,2020,0(21):3956-3962.
作者姓名:胡云华  王仁举  张子怡  孙立明  丁玉松  芮东升  牛强  宋关玲  郭淑霞  李述刚
作者单位:1.石河子大学医学院预防医学系,新疆 石河子 832000;2.首都医科大学公共卫生学院,北京市 丰台区 100069
摘    要:目的 通过Meta分析探讨在砷在诱导细胞凋亡过程中JNK1/2信号通路发挥的作用及机制。 方法 在CNKI、维普、万方、SinoMed、PubMed、Web of Science、Cochrane、Spinger等数据库中检索文献。采用STAIR清单对文献质量进行评价,应用Stata 12.0和RevMan 5.3软件提取数据及分析;以标准化均数差(SMD)来描述其组间差别。 结果 本研究共纳入33篇文献。砷干预组Bax:SMD=9.41,95%CI(1.92,16.90),凋亡细胞:SMD=10.46,95%CI(6.87,14.05),Caspase-3:SMD=8.82,95%CI(0.79,16.85),Cytochrome C:SMD=90.24,95%CI(34.45,146.03),c-jun:SMD=81.66,95%CI(14.38,148.94)和P-JNK:SMD=139.06,95%CI(29.14,248.98)水平均高于对照组。Bcl-2:SMD=-3.78,95%CI(-7.17,-0.39)和PARP:SMD=-6.48,95%CI(-12.89,-0.07)的水平均低于对照组。亚组分析表明正常细胞中高剂量(>5μmol)且长时间(≥24h)砷暴露可抑制JNK1和JNK2的蛋白表达,在癌细胞中低剂量(≤5μmol)且短时间(<24h)砷暴露则会诱导JNK1和JNK2的表达。 结论 砷通过介导JNK1/2信号通路诱导细胞凋亡,且作用效果与细胞类型、作用时间和剂量有关。

关 键 词:  细胞凋亡  JNK  Meta分析

Meta-analysis of bipartite effects of JNK1/2 signaling pathway in arsenic induced apoptosis
HU Yun-hua,WANG Ren-ju,ZHANG Zi-yi,SUN Li-ming,DING Yu-song,RUI Dong-sheng,NIU Qiang,SONG Guan-ling,GUO Shu-xia,LI Shu-gang.Meta-analysis of bipartite effects of JNK1/2 signaling pathway in arsenic induced apoptosis[J].Modern Preventive Medicine,2020,0(21):3956-3962.
Authors:HU Yun-hua  WANG Ren-ju  ZHANG Zi-yi  SUN Li-ming  DING Yu-song  RUI Dong-sheng  NIU Qiang  SONG Guan-ling  GUO Shu-xia  LI Shu-gang
Institution:*Department of Prevention Medicine, Medical School of Shihezi University, Shihezi, Xinjiang 832000, China
Abstract:Abstract: Objective To investigate the role and mechanism of JNK1 /2 signaling pathway in inducing apoptosis. Methods Relevant studies were searched in databases such as CNKI,VIP,WanFang,SinoMed,PubMed,Web of Science,Cochrane,and Spinger. Stata12. 0 and RevMan5. 3 software were used to extract data for analysis. STAIR checklist was used to evaluate the quality of the literatures,and SMD was used to describe differences between groups. Results A total of 33 literatures were included in this study. The Bax: SMD = 9. 41,95% CI ( 1. 92,16. 90) ,apoptotic cell: SMD = 10. 46,95% CI ( 6. 87,14. 05) ,Caspase - 3: SMD = 8. 82,95% CI ( 0. 79,16. 85) ,Cytochrome C: SMD = 90. 24,95% CI ( 34. 45,146. 03) ,c -jun: SMD = 81. 66,95% CI ( 14. 38,148. 94) and P - JNK: SMD = 139. 06,95% CI ( 29. 14,248. 98) levels in the arsenic intervention group were higher than the control group. While the levels of Bcl - 2: SMD = - 3. 78,95% CI ( - 7. 17,- 0. 39)and PARP: SMD = - 6. 48,95% CI ( - 12. 89,- 0. 07) were lower than the control group. Subgroup analysis showed that high - dose ( > 5μmol) and long - term ( ≥24h) arsenic exposure in normal cells could inhibit JNK1 and JNK2 protein expressions. Low - dose ( ≤5μmol) and short - term ( < 24h) arsenic exposure in cancer cells could induce the expressions ofJNK1 and JNK2. Conclusion Arsenic induces apoptosis by mediating the JNK1 /2 signaling pathway,and the effect is related to cell type,duration of action,and dose.
Keywords:Arsenic  Apoptosis  JNK  Meta - analysis
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