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MitoQ 补充剂可预防母亲吸烟对雄性小鼠后代肾脏发育、氧化应激和线粒体密度的长期影响。

MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring.

机构信息

School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, 2007, Australia.

Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.

出版信息

Sci Rep. 2018 Apr 26;8(1):6631. doi: 10.1038/s41598-018-24949-0.

DOI:10.1038/s41598-018-24949-0
PMID:29700332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5919980/
Abstract

To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many diseases. Female Balb/c mice (8 weeks) were divided into Sham (exposed to air), SE (exposed to cigarette smoke) and SEMQ (exposed to cigarette smoke with MitoQ supplemented from mating) groups. Kidneys from the mothers were collected when the pups weaned and those from the offspring were collected at 13 weeks. Maternal MitoQ supplementation during gestation and lactation significantly reversed the adverse impact of maternal SE on offspring's body weight, kidney mass and renal pathology. MitoQ administration also significantly reversed the impact of SE on the renal cellular mitochondrial density and renal total reactive oxygen species in both the mothers and their offspring in adulthood. Our results suggested that MitoQ supplementation can mitigate the adverse impact of maternal SE on offspring's renal pathology, renal oxidative stress and mitochondrial density in mice offspring.

摘要

为了研究母源性 MitoQ 处理对母体吸烟暴露(SE)引起的肾脏疾病的影响。我们已经证明,妊娠期间母体 SE 会增加成年后代发生慢性肾脏病(CKD)的风险。线粒体氧化损伤导致母体吸烟对肾脏疾病的不良影响。MitoQ 是一种线粒体靶向抗氧化剂,已被证明可预防许多疾病中与氧化损伤相关的病理学。将 8 周龄的雌性 Balb/c 小鼠分为假手术组(暴露于空气中)、SE 组(暴露于香烟烟雾中)和 SEMQ 组(与香烟烟雾暴露并用 MitoQ 补充从交配开始)。当幼崽断奶时,从母亲身上收集肾脏,从 13 周龄的后代身上收集肾脏。妊娠和哺乳期的母源性 MitoQ 补充显著逆转了母体 SE 对后代体重、肾脏质量和肾脏病理学的不良影响。SE 对成年母体和后代肾脏细胞线粒体密度和肾脏总活性氧的影响也显著被 MitoQ 处理逆转。我们的研究结果表明,MitoQ 补充可以减轻母体 SE 对后代肾脏病理学、肾脏氧化应激和线粒体密度的不良影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/028899b67f74/41598_2018_24949_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/09d997cdab9d/41598_2018_24949_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/43e7bfa87941/41598_2018_24949_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/b7f14768de99/41598_2018_24949_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/b60c29317cd8/41598_2018_24949_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/028899b67f74/41598_2018_24949_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/09d997cdab9d/41598_2018_24949_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/43e7bfa87941/41598_2018_24949_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/b7f14768de99/41598_2018_24949_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/b60c29317cd8/41598_2018_24949_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/5919980/028899b67f74/41598_2018_24949_Fig5_HTML.jpg

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