期刊文献+

重性抑郁障碍患者他克莫司结合蛋白5基因多态性分析

Tacrolimus binding proteins 5 gene polymorphisms in major depressive disorder
原文传递
导出
摘要 目的 分析中国汉族重性抑郁障碍患者他克莫司结合蛋白5(FKBP5)基因多态性.方法 对符合《美国诊断与统计手册精神障碍(第4版)》(DSM-Ⅳ)重性抑郁障碍诊断标准的263例患者予以单一抗抑郁药治疗,疗程6周.根据汉密尔顿抑郁量表(HAMD)评分,在治疗6周末将患者分为有效组(HAMD减分率≥50%)和无效组(HAMD减分率<50%).入组时取患者血液标本提取DNA,采用高温连接酶检测反应法(LDR)检测FKBP5基因的rs3800373和rs1360780两个位点.结果 (1)有效组FKBP5基因rs3800373位点GG+ GT、TT基因型频率分别为45.7%、54.3%,无效组分别为47.6%、52.4%,两组比较差异无统计学意义(x2=0.051,P>0.05);有效组FKBP5基因rs1360780位点CC、CT +TT基因型频率分别为55.6%、44.4%,无效组分别为51.2%、48.8%,两组比较差异无统计学意义(x2=0.256,P>0.05);(2)有效组和无效组的rs3800373-rs1360780两位点单倍型分布差异无统计学意义(P >0.05);(3) rs3800373、rs1360780两位点不同基因型患者之间总不良反应发生率及恶心不良反应发生率比较差异均无统计学意义(P>0.05).结论 未发现中国汉族重性抑郁障碍患者不同疗效组患者FKBP5基因rs3800373、rs1360780两位点分布存在差异. Objective Tacrolimus binding proteins 5 (FKBP5) gene polymorphisms were analyzed in Chinese Han major depressive disorder (MDD) patients.Methods 263 major depressive disorder (MDD) patients who met the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM-Ⅳ)criterion were given antidepressant drugs for six weeks.The patients were divided into two groups of the responder group and the non-responder group,according to the decreasing rate of score of HAMD ≥ 50%and 〈 50% respectively.Genomic DNA was extracted from the blood samples,when patients being enrolled.Two polymorphisms (rs3800373 and rs1360780) of FKBP5 gene were genotyped using the ligase detection reaction.Results (1)The distribution frequencies of the SNP of rs3800373 showed no significant differences between responder group (GG + GT 45.7% ; TT 54.3%) and non-responder group (GG + GT47.6% ;T T 52.4%) (x2 =0.051,P 〉 0.05).The distribution frequencies of the SNP of rs1360780 showed no significant differences between responder group(CC 55.6% ; CT + TF 44.4%) and non-responder group (CC 51.2% ; CT + TT 48.8%) (x2 =0.256,P 〉 0.05).(2) No significant differences were found in rs3800373-rs1360780 haplotype frequencies between responder group and non-responder group (P 〉 0.05).(3) There were no significant differences in the incidence rate of total side effect and nausea adverse effect between the patients with different genotypes of rs3800373 and rs1360780 (P 〉 0.05).Conclusions There may be no significant differences in the genotype frequencies of FKBP5 gene rs3800373 and rs1360780 polymorphisms between responder group and non-responder group in Chinese Han MDD patients.
出处 《中华精神科杂志》 CAS CSCD 北大核心 2013年第5期285-289,共5页 Chinese Journal of Psychiatry
基金 国家十五攻关课题(2004DA7210A21)
关键词 抑郁症 他克莫司结合蛋白质类 基因 多态性 限制性片段长度 Depressive disorder Tacrolimus binding proteins Genes Polymorphism,restriction fragment length
  • 相关文献

参考文献12

  • 1Nikisch G. Involvement and role of antidepressant drugs of the hypothalamic-pituitary-adrenal axis and glueoeorticoid receptor function. Neuro Endocrinol Lett ,2009,30 : 11-16.
  • 2Sehosser A, Kasper S. The role of pharmacogeneties in the treatment of depression and anxiety disorders. Int Clin Psychopharmaeol, 2009,24 : 277 -288.
  • 3Spijker AT, van Rossum EF. Glueoeorticoid sensitivity in mood disorders. Neuroendoerinology ,2012,95 : 179-186.
  • 4Binder EB. The role of FKBP5, a co-chaperone of the glueocorticoid receptor in the pathogenesis and therapy of affeetive and anxiety disorders. Psyehoneuroendocrinology, 2009,34 Suppl 1 :S186-195.
  • 5喻妍,赵靖平,杨栋,吴仁容,郭文斌.他克莫司结合蛋白5基因多态性与抑郁症的关联研究[J].中华精神科杂志,2012,45(4):218-222. 被引量:1
  • 6Wochnik GM, Riiegg J, Abel GA, et al, FKS06-binding proteins 51 and 52 differentially regulate dynein interaction and nucleartranslocation of the glucocorticoid receptor in mammalian cells. J Biol Chem,2005,280:4609-4616.
  • 7Westberry JM, Sadosky PW, Hubler TR, et al. Glucocortieoid resistance in squirrel monkeys results from a combination of a transcriptionally incompetent glucocorticoid receptor and overexpression of the glucocorticoid receptor co-chaperone FKBP51. J Steroid Biochem Mol Biol,2006,100 ( 1-3 ) : 34-41.
  • 8Binder EB, Salyakina D, Lichtner P, et al. Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment. Nat Genet,2004,36 : 1319-1325.
  • 9Lekman M, Laje G, Charney D, et al. The FKBP5-gene in depression and treatment response: an association study in the Sequenced Treatment Alternatives to Relieve Depression ( STAR * D) Cohort. Biol Psychiatry,2008,63 : 1103-1110.
  • 10Kirchheiner J, Lorch R, Lebedeva E, et al. Genetic variants in FKBP5 affecting response to antidepressant drug treatment. Pharmacogenomics, 2008,9 : 841-846.

二级参考文献14

  • 1刘晓华,江开达,徐一峰,江三多.抑郁症分子遗传学的研究进展[J].中华精神科杂志,2006,39(4):240-243. 被引量:4
  • 2Vermeer H, Hendriks-Stegeman BI, van der Burg B, et al. Glucocorticoid-induced increase in lymphocytic FKBP51 messenger ribonucleic acid expression: a potential marker for glucocorticoid sensitivity, potency, and bioavailability. J Clin Endocrinol Metab, 2003, 88:277-284.
  • 3Brent D, Melhem N, Ferrell R, et al. Association of FKBP5 polymorphisms with suicidal events in the Treatment of Resistant Depression in Adolescents (TORDIA) study. Am J Psychiatry, 2010,167 : 190-197.
  • 4Binder EB, Salyakina D, Lichtner P, et al. Polymorphisms in FKBP5 are associated with inereased recurrence of depressive episodes and rapid response to antidepressant treatment. Nat Genet, 2004, 36:1319-1325.
  • 5Papiol S, Arias B, Gast6 C, et al. Genetic variability at HPA axis in major depression and clinical response to antidepressant treatment. J Affect Disord, 2007, 104(1-3) : 83-90.
  • 6Gawlik M, Moller-Ehrlieh K, Mende M, et al. Is FKBP5 a genetic marker of affective psychosis? A case control study and analysis of disease related traits. BMC Psychiatry, 2006, 6:52.
  • 7Lekman M, Laje G, Chamey D, et al. The FKBP5-gene in depression and treatment response-an association study in the Sequenced Treatment Alternatives to Relieve Depression ( STAR * D) Cohort. Biol Psychiatry, 2008, 63 : 1103-1110.
  • 8Willour VL, Chen H, Toolan J, et al. Family-based association of FKBP5 in bipolar disorder. Mol Psychiatry, 2009, 14: 261-268.
  • 9Wochnik GM, Ruegg J, Abel GA, et al. FKS06-binding proteins 51 and 52 differentially regulate dynein interaction and nuclear translocation of the glucocorticoid receptor in mammalian cells. J Biol Chem, 2005, 280: 4609-4616.
  • 10Westberry JM, Sadosky PW, Hubler TR, et al. Glucocorticoid resistance in squirrel monkeys results from a combination of a transcriptionally incompetent glucocorticoid receptor and overexpression of the glucocorticoid receptor co-chaperone FKBP51. J Steroid Biochem Mol Biol, 2006, 100 ( 1-3 ) : 34-41.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部