Scholarlink

<p>Prenatal exposure to a high-fat diet (HFD) or microplastics can impact liver fat accumulation in offspring. This study investigates the protective effects of prenatal melatonin on liver injury in male pups resulting from maternal exposure to a HFD and microplastics. Pregnant Sprague-Dawley rats were fed either an HFD or a normal chow diet, with some groups exposed to microplastics alone or in combination with melatonin. Male pups were evaluated on postnatal day 7. Results indicated that pups in the HFD-microplastics group (HFD-Mi) exhibited increased liver lipid accumulation (observed in histological staining), apoptosis (elevated cleaved caspase 3, phospho-AKT, and TUNEL staining), inflammation (higher IL- 6 and TNF-α), and oxidative stress (elevated malondialdehyde). Conversely, melatonin treatment (HFD-Mi + M) significantly reduced these effects, including lipid accumulation, apoptosis, and inflammation, while enhancing antioxidant enzyme glutathione peroxidase activity and improving lipid metabolism (reduced SREBP- 1 expression). These findings suggest that prenatal melatonin mitigates liver injury caused by maternal HFD and microplastics through its anti-inflammatory, antioxidative, and lipid-regulating properties, underscoring its potential hepatoprotective role.</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 melatonin reprograms liver injury in male pups caused by maternal exposure to a high-fat diet and microplastics

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月11日

查看全文
  • Yu-Jen Chen,
  • Hong-Ren Yu,
  • Ching-Chou Tsai,
  • Mao-Meng Tiao

摘要

Prenatal exposure to a high-fat diet (HFD) or microplastics can impact liver fat accumulation in offspring. This study investigates the protective effects of prenatal melatonin on liver injury in male pups resulting from maternal exposure to a HFD and microplastics. Pregnant Sprague-Dawley rats were fed either an HFD or a normal chow diet, with some groups exposed to microplastics alone or in combination with melatonin. Male pups were evaluated on postnatal day 7. Results indicated that pups in the HFD-microplastics group (HFD-Mi) exhibited increased liver lipid accumulation (observed in histological staining), apoptosis (elevated cleaved caspase 3, phospho-AKT, and TUNEL staining), inflammation (higher IL- 6 and TNF-α), and oxidative stress (elevated malondialdehyde). Conversely, melatonin treatment (HFD-Mi + M) significantly reduced these effects, including lipid accumulation, apoptosis, and inflammation, while enhancing antioxidant enzyme glutathione peroxidase activity and improving lipid metabolism (reduced SREBP- 1 expression). These findings suggest that prenatal melatonin mitigates liver injury caused by maternal HFD and microplastics through its anti-inflammatory, antioxidative, and lipid-regulating properties, underscoring its potential hepatoprotective role.