摘要
目的探讨高脂饮食喂养对雄性C57/BL6小鼠肺部组织的氧化应激损伤和Klotho甲基化调控机制。方法选用4周龄雄性C57/BL6小鼠,对照组喂普通饲料,高脂组喂高脂饲料,共喂养10周。两组动物处死后取肺部组织匀浆后用试剂盒检测超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA)。qPCR检测肺组织klotho基因表达情况,蛋白印记(Western-blot)检测肺组织klotho蛋白表达。甲基化特异性PCR(MS-PCR)检测肺组织klotho甲基化状态。结果相对于对照组,高脂组肺组织出现了较高水平的氧化应激,高脂组肺组织klotho的mRNA和蛋白表达均降低,klotho基因启动子甲基化水平升高。结论高脂饮食可以导致C57/BL6小鼠肺组织氧化应激损伤,klotho启动子甲基化可以在其中扮演着重要角色。
Objective To investigate the effect of high-fat diet-induced obesity on oxidative stress and klotho promoter methylation in lung tissue of C57/BL6 mice. Methods Mice in the control group were feed with the normal diet, and mice in the obesity group were feed with high-fat diet. The lung tissue level of uperoxide dis- mutase （SOD） and malondialdehyde （MDA） were determined by using mice enzyme-linked immunosorbent assay （ELISA） kit. The klotho mRNA and protein expression was determined by qPCR and Western-blot, respectively. The Klotho gene methylation status was determined by methylation specific PCR （MS-PCR）. Results Compared with the control group, mice in the obesity group had high level of oxidative stress in lung tissue. Meanwhile, mice in the experimental group had lower levels of klotho mRNA and protein expression than those in the control group. The high-fat diet increased the degree of Klotho gene methylation. Conclusion High-fat diet could lead injure in lung tissue in C57/BL6 mice, klorho promoter methylation may play an important role involved in the process.
出处
《实用医学杂志》
CAS
北大核心
2017年第18期3017-3020,共4页
The Journal of Practical Medicine
基金
四川省卫计委课题"SIRT2在非小细胞肺癌中的表达及其分子机制研究"(编号:17PJ045)
