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作 者:潘竞 覃远汉[1] 蒋玲[1] 席志杨 涂立 蹇淑娟 PAN Jing;QIN Yuan-han;JIANG Ling;XI Zhing-yang;TU Li;JIAN Shu-juan(The First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China)
机构地区:[1]广西医科大学第一附属医院儿科,广西南宁530021
出 处:《广东医学》2021年第6期657-660,共4页Guangdong Medical Journal
基 金:广西自然科学基金资助项目(2017GXNSFDA198008)。
摘 要:目的从表观遗传学范畴探讨过氧化物酶体增殖物激活受体γ(peroxisome proliferator aetivated receptor gamma,PPARγ)甲基化可能参与肾间质纤维化(renal interstitial fibrosis,RIF)发生、发展的机制,为慢性肾脏病的治疗提供新思路。方法选取健康儿童51例(正常组)、经肾脏穿刺活检术后诊断为慢性肾脏病患儿75例,其中病理诊断为RIF和非RIF分别为33例(RIF组)和42例(非RIF组),取抗凝血提取基因组DNA,采用重亚硫酸盐扩增子测序的方法分别检测各组PPARγ基因第71、第85、第163、第257位点甲基化状态。结果在第71和85两个位点间,RIF组和非RIF组PPARγ基因甲基化比例均显著低于正常组(P均<0.05),但在RIF组和非RIF组之间差异无统计学意义(P>0.05)。而第163及257两个位点,3组之间均差异无统计学意义(P>0.05)。结论PPARγ甲基化水平降低可能在RIF出现前已发生,PPARγ低甲基化可能参与慢性肾脏病发生、发展。Objective To investiagate the mechanism of peroxisome proliferator activated receptorγ(PPARγ)methylation involved in the development of renal interstitial fibrosis from the perspective of epigenetics,so as to provide new ideas for the treatment of chronic kidney disease.Methods Fifty-one healthy children and 75 children with chronic kidney disease after renal biopsy were enrolled.The pathological manifestations of RIF and non-RIF were 33 and 42,respectively.The genomic DNA was extracted from anticoagulant,and the methylation status of the 71st,85th,163rd and 257th sites of PPARγ gene in each group was detected by the method of bisulfite amplicon sequencing.Results The PPARγ gene of RIF group and non RIF group was significantly lower than that of normal group(P<0.05),but there was no significant difference between RIF group and non RIF group(P>0.05),while there was no significant difference between the 163rd and 257th sites(P>0.05).Conclusion The decrease of PPARγ methylation may have occurred before RIF,and the hypomethylation of PPARγ may be involved in the development of chronic kidney disease.
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