Department of Gynecology and Obstetrics, Affiliated Dongguan People's Hospital, Southern Medical University, Dongguan 523059, China.
Department of Obstetrics and Gynecology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China.
Chem Res Toxicol. 2021 Jan 18;34(1):47-53. doi: 10.1021/acs.chemrestox.0c00056. Epub 2021 Jan 4.
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.
颗粒物 (PM2.5) 暴露被报道对健康有有害影响。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,我们旨在研究宫内 PM2.5 暴露对早产体重和出生后肺发育的影响。怀孕的 Sprague-Dawley 大鼠每隔 3 天通过腹膜内注射给予 PM2.5(0.1、0.5、2.5 或 7.5 mg/kg),直到分娩。监测母体和出生结果以及体细胞生长。在 PND1(其中 PND = 出生后日)和 PND28 收集肺;分析肺湿重/干重比(W/D),并测量活性氧 (ROS) 水平。通过 Western blot 和定量 RT-PCR 评估 Toll 样受体 4 (TLR4) 和 NF-κB 的表达。母体结果没有明显的组间差异;然而,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。宫内暴露于 2.5 和 7.5 mg/kg PM2.5 导致出生后体重降低,并破坏婴儿期的肺发育。7.5 mg/kg PM2.5 组的 ROS 水平显着升高。PM2.5 处理的大鼠显示肺 TLR4 和 NF-κB 的表达上调。母体 PM2.5 暴露增加了低出生体重的风险,并影响了肺肺泡的发育。潜在的分子机制可能涉及 TLR4/NF-κB 信号通路。