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作 者:张辉[1] 王红艳 彭思涵 梁小利[1] 曹冰 张先庚[1,2]
机构地区:[1]成都中医药大学护理学院,成都611137 [2]四川护理职业学院,成都610100
出 处:《中华中医药杂志》2016年第11期4499-4501,共3页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金项目(No.81373710);成都中医药大学科技发展基金项目(No.ZRQN1541)~~
摘 要:目的:研究金匮肾气丸防治SD孕鼠创伤后压力心理障碍(PTSD)所致胎损的表观遗传机制。方法:将首次受孕的36只孕鼠随机分为3组,每组12只。采用SPS法构建PTSD模型,金匮肾气丸混合饲料补肾。采用表达谱芯片检测30龄子鼠的基因表达情况,Me DIP-Seq对全基因组进行甲基化测序。结果:经表达谱芯片结果与甲基化测序结果联合分析,孕鼠模拟PTSD使得子鼠的的Ntf3基因成高甲基化状态从而抑制该基因的表达。金匮肾气丸治疗后可使得该基因的甲基化水平回复正常从而解除对该基因表达的抑制。结论:Ntf3基因的高甲基化状态可能是孕鼠PTSD胎损的表观遗传学机制,也是金匮肾气丸补肾干预起效的关键环节,为进一步研究中医调护PTSD胎损的表观遗传学机制奠定了基础。Objective: To study the epigenetic mechanism of Jingui Shenqi Pill(JGSQP) in treating the negative influence on offspring from pregnant rat with post-traumatic stress disorder(PTSD). Methods: 36 initial pregnant SD rats were randomly divided into 3 groups with 12 rats in each group. SPS was applied to modulate PTSD. JGSQP was mixed into ordinary feed to invigorate the kidney. Gene expression profile chip(GEPC) was utilized to test the gene expression, and Me DIP-Seq was utilized to sequence the whole genome methylation of the offspring on 30 days after birth. Results: Ntf3 was screened through the joint-analysis with GEPC and Me DIP-Seq. PTSD caused the hyper-methylation of Ntf3 in the offspring, which suppressed the expression of the gene. After treatment with JGSQP, the hyper-methylation was neutralized and the gene expression level of Ntf3 was normalized. Conclusion: The hyper-methylation of Ntf3 could be the mechanism of fetus injury resulting from PTSD, which plays an important role in the kidney-invigorating effect of JGSQP, and it lays the foundation for further research on epigenetics mechanism of TCM in treating negative influence on offspring from pregnant rat with PTSD.
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