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In Utero Exposure to Fine Particles Decreases Early Birth Weight of Rat Offspring and TLR4/NF-κB Expression in Lungs
Chemical Research in Toxicology ( IF 4.1 ) Pub Date : 2021-01-04 , DOI: 10.1021/acs.chemrestox.0c00056
Wenting Tang 1, 2 , Zhongjun Li 1 , Yaoguang Huang 3 , Lili Du 2 , Chuangyu Wen 1 , Wen Sun 2 , Zhiqiang Yu 4 , Suran Huang 1 , Dunjin Chen 2
Affiliation  

Particulate matter (PM2.5) exposure is reported to have deleterious effects on health. Maternal PM2.5 exposure has been confirmed to damage the growth of somatic cells and enhance the incidence of chronic respiratory diseases in children. Here we aim to investigate the impact of in utero PM2.5 exposure on early birth weight and postnatal lung development. Pregnant Sprague–Dawley rats were administered PM2.5 (0.1, 0.5, 2.5, or 7.5 mg/kg) intraperitoneally every 3 days until birth. Maternal and birth outcomes and somatic growth were monitored. Lungs were collected on PND1 (where PND = postnatal day) and PND28; the lung wet-to-dry weight ratio (W/D) was analyzed, and reactive oxygen species (ROS) levels were measured. Expression of Toll-like receptor 4 (TLR4) and NF-κB were evaluated by Western blotting and quantitative RT-PCR. There were no significant intergroup differences for maternal outcomes; however, offspring exposed in utero to 2.5 and 7.5 mg/kg PM2.5 were significantly smaller in litter weight than the controls. In utero exposure to 2.5 and 7.5 mg/kg PM2.5 led to lower body weight after birth and disrupted lung development during infancy. ROS levels were significantly increased in the 7.5 mg/kg PM2.5 group. PM2.5-treated rats showed upregulated pulmonary expression of TLR4 and NF-κB. Maternal PM2.5 exposure enhances the risk of low birth weight and affects lung alveolar development. The underlying molecular mechanisms may involve TLR4/NF-κB signaling.

中文翻译:

在子宫内暴露于细颗粒会降低大鼠后代的早期出生体重和肺中 TLR4/NF-κB 的表达

据报道,颗粒物 (PM2.5) 暴露会对健康产生有害影响。母体PM2.5暴露已被证实会损害体细胞的生长并增加儿童慢性呼吸道疾病的发病率。在这里,我们旨在调查宫内 PM2.5 暴露对早期出生体重和出生后肺发育的影响。怀孕的 Sprague-Dawley 大鼠每 3 天腹膜内注射 PM2.5(0.1、0.5、2.5 或 7.5 mg/kg)直至出生。监测孕产妇和分娩结果以及体细胞生长。在 PND1(其中 PND = 产后天)和 PND28 上收集肺;分析了肺湿干重比 (W/D),并测量了活性氧 (ROS) 水平。通过蛋白质印迹和定量 RT-PCR 评估 Toll 样受体 4 (TLR4) 和 NF-κB 的表达。产妇结局没有显着的组间差异;然而,在子宫内暴露于 2.5 和 7.5 mg/kg PM2.5 的后代的窝重明显小于对照组。在子宫内暴露于 2.5 和 7.5 毫克/千克 PM2.5 会导致出生后体重降低,并在婴儿期破坏肺发育。7.5 mg/kg PM2.5 组的 ROS 水平显着增加。PM2.5 处理的大鼠表现出 TLR4 和 NF-κB 的肺表达上调。母亲暴露于 PM2.5 会增加低出生体重的风险并影响肺泡发育。潜在的分子机制可能涉及 TLR4/NF-κB 信号传导。5 mg/kg PM2.5 导致出生后体重降低,并在婴儿期破坏肺发育。7.5 mg/kg PM2.5 组的 ROS 水平显着增加。PM2.5 处理的大鼠表现出 TLR4 和 NF-κB 的肺表达上调。母亲暴露于 PM2.5 会增加低出生体重的风险并影响肺泡发育。潜在的分子机制可能涉及 TLR4/NF-κB 信号传导。5 mg/kg PM2.5 导致出生后体重降低,并在婴儿期破坏肺发育。7.5 mg/kg PM2.5 组的 ROS 水平显着增加。PM2.5 处理的大鼠表现出 TLR4 和 NF-κB 的肺表达上调。母亲暴露于 PM2.5 会增加低出生体重的风险并影响肺泡发育。潜在的分子机制可能涉及 TLR4/NF-κB 信号传导。
更新日期:2021-01-18
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