Scholarlink

<p>As a widely used plasticizer, diisononyl phthalate (DINP) has been considered an emerging environmental pollutant. Epidemiological evidence shows that prenatal DINP exposure is linked to an increased risk of lung diseases in offspring and adults. However, little is known about their relationship at the molecular level. We exposed pregnant mice to DINP (100&#xa0;mg/kg/day) by intragastric administration throughout gestation. On postnatal days (PNDs) 21 and 42, offspring were sacrificed and the lungs were collected. We found that prenatal DINP exposure significantly caused hypoalveolarization in male offspring on PND 21, which was reversed during postnatal development. Moreover, prenatal DINP exposure significantly caused pulmonary fibrosis in male offspring on PND 42. However, neither of these changes was observed in female offspring. KEGG enrichment showed that differentially expressed genes (DEGs) in the lungs of male offspring were closely associated with the calcium signaling and IL-17 signaling pathways. Importantly, decreased <i>Htr4</i> expression might contribute to hypoalveolarization, and the elevated <i>Il-17a</i> expression might be responsible for prenatal DINP exposure-induced pulmonary fibrosis in male offspring. Our results demonstrated that prenatal DINP exposure had a persistent impact on lung development in male offspring, including early-stage impaired alveolarization and later-stage fibrosis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Prenatal diisononyl phthalate exposure induces the development of pulmonary dysplasia in offspring

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月3日

查看全文
  • Dan Li,
  • Chengyu Zhao,
  • Fu Xu,
  • Yao Yuan,
  • Sihan Zhang,
  • Yuanyuan Tian,
  • Meiqiong Wu

摘要

As a widely used plasticizer, diisononyl phthalate (DINP) has been considered an emerging environmental pollutant. Epidemiological evidence shows that prenatal DINP exposure is linked to an increased risk of lung diseases in offspring and adults. However, little is known about their relationship at the molecular level. We exposed pregnant mice to DINP (100 mg/kg/day) by intragastric administration throughout gestation. On postnatal days (PNDs) 21 and 42, offspring were sacrificed and the lungs were collected. We found that prenatal DINP exposure significantly caused hypoalveolarization in male offspring on PND 21, which was reversed during postnatal development. Moreover, prenatal DINP exposure significantly caused pulmonary fibrosis in male offspring on PND 42. However, neither of these changes was observed in female offspring. KEGG enrichment showed that differentially expressed genes (DEGs) in the lungs of male offspring were closely associated with the calcium signaling and IL-17 signaling pathways. Importantly, decreased Htr4 expression might contribute to hypoalveolarization, and the elevated Il-17a expression might be responsible for prenatal DINP exposure-induced pulmonary fibrosis in male offspring. Our results demonstrated that prenatal DINP exposure had a persistent impact on lung development in male offspring, including early-stage impaired alveolarization and later-stage fibrosis.