Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
Chang Gung Medical Education Research Centre, Chang Gung Memorial Hospital, Linkou, Taoyuan 333, Taiwan.
Int J Mol Sci. 2023 Aug 30;24(17):13457. doi: 10.3390/ijms241713457.
Prenatal high-fat diet (HFD) or exposure to microplastics can affect the accumulation of liver fat in offspring. We sought to determine the effects of maternal HFD intake and microplastic exposure on fatty liver injury through oxidative stress in pups. Pregnant female Sprague-Dawley rats were randomly divided into maternal HFD (experimental group) or normal control diet (NCD; control group) groups with or without microplastic exposure. As a result, the following groups were established: HFD-L (HFD + microplastics, 5 µm, 100 μg/L), HFD-H (HFD + microplastics, 5 µm, 1000 μg/L), NCD-L (NCD + microplastics, 5 µm, 100 μg/L), and NCD-H (NCD + microplastics, 5 µm, 1000 μg/L). The pups were sacrificed on postnatal day 7 (PD7). Liver histology revealed increased hepatic lipid accumulation in pups in the HFD-L and HFD-H groups compared to those in the HFD, NCD-L, NCD-H, and NCD groups on PD7. Similarly, liver TUNEL staining and cellular apoptosis were found to increase in pups in the HFD-L and HFD-H groups compared to those in the HFD, NCD-L, NCD-H, and NCD groups. The expression levels of malondialdehyde, a lipid peroxidation marker, were high in the HFD, HFD-L, and HFD-H groups; however, the highest expression was observed in the HFD-H group ( < 0.05). The levels of glutathione peroxidase, an antioxidant enzyme, decreased in the HFD, HFD-L, and HFD-H groups ( < 0.05). Overall, oxidative stress with cellular apoptosis plays a vital role in liver injury in offspring after maternal intake of HFD and exposure to microplastic; such findings may shed light on future therapeutic strategies.
产前高脂肪饮食（HFD）或暴露于微塑料会影响后代肝脏脂肪的积累。我们试图通过幼崽的氧化应激来确定母体 HFD 摄入和微塑料暴露对脂肪肝损伤的影响。将怀孕的雌性 Sprague-Dawley 大鼠随机分为母体 HFD（实验组）或正常对照饮食（NCD；对照组）组，并进行或不进行微塑料暴露。结果建立了以下组：HFD-L（HFD+微塑料，5 µm，100 µg/L）、HFD-H（HFD+微塑料，5 µm，1000 µg/L）、NCD-L（NCD+微塑料，5 µm，100 µg/L）和 NCD-H（NCD+微塑料，5 µm，1000 µg/L）。幼崽于产后第 7 天（PD7）被处死。肝组织学显示，与 HFD、NCD-L、NCD-H 和 NCD 组相比，HFD-L 和 HFD-H 组的 PD7 幼崽肝脏脂质积累增加。同样，与 HFD、NCD-L、NCD-H 和 NCD 组相比，HFD-L 和 HFD-H 组的幼崽肝组织 TUNEL 染色和细胞凋亡增加。丙二醛（脂质过氧化标志物）的表达水平在 HFD、HFD-L 和 HFD-H 组中较高；然而，在 HFD-H 组中观察到最高表达（<0.05）。抗氧化酶谷胱甘肽过氧化物酶的水平在 HFD、HFD-L 和 HFD-H 组中降低（<0.05）。总的来说，母体摄入 HFD 和暴露于微塑料后，氧化应激伴细胞凋亡在子代肝脏损伤中发挥重要作用；这些发现可能为未来的治疗策略提供启示。
