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过氧化物酶体增殖物激活受体 γ 调节三氯生诱导的胎盘功能障碍。

PPARγ Regulates Triclosan Induced Placental Dysfunction.

机构信息

School of Public Health, Xuzhou Medical University, 209 Tong-Shan Road, Xuzhou 221002, China.

Key Laboratory of Human Genetics and Environmental Medicine, Xuzhou Medical University, Xuzhou 221004, China.

出版信息

Cells. 2021 Dec 28;11(1):86. doi: 10.3390/cells11010086.

DOI:10.3390/cells11010086
PMID:35011648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8750171/
Abstract

Exposure to the antibacterial agent triclosan (TCS) is associated with abnormal placenta growth and fetal development during pregnancy. Peroxisome proliferator-activated receptor γ (PPARγ) is crucial in placenta development. However, the mechanism of PPARγ in placenta injury induced by TCS remains unknown. Herein, we demonstrated that PPARγ worked as a protector against TCS-induced toxicity. TCS inhibited cell viability, migration, and angiogenesis dose-dependently in HTR-8/SVneo and JEG-3 cells. Furthermore, TCS downregulated expression of PPARγ and its downstream viability, migration, angiogenesis-related genes , , , , , and upregulated inflammatory genes , , , and in vitro and in vivo. Further investigation showed that overexpression or activation (rosiglitazone) alleviated cell viability, migration, angiogenesis inhibition, and inflammatory response caused by TCS, while knockdown or inhibition (GW9662) of PPARγ had the opposite effect. Moreover, TCS caused placenta dysfunction characterized by the significant decrease in weight and size of the placenta and fetus, while PPARγ agonist rosiglitazone alleviated this damage in mice. Taken together, our results illustrated that TCS-induced placenta dysfunction, which was mediated by the PPARγ pathway. Our findings reveal that activation of PPARγ might be a promising strategy against the adverse effects of TCS exposure on the placenta and fetus.

摘要

接触抗菌剂三氯生（TCS）与怀孕期间异常的胎盘生长和胎儿发育有关。过氧化物酶体增殖物激活受体γ（PPARγ）在胎盘发育中至关重要。然而，TCS 诱导的胎盘损伤中 PPARγ的机制尚不清楚。在此，我们证明 PPARγ可作为 TCS 诱导的毒性的保护剂。TCS 以剂量依赖性方式抑制 HTR-8/SVneo 和 JEG-3 细胞中的细胞活力、迁移和血管生成。此外，TCS 下调了 PPARγ及其下游与活力、迁移、血管生成相关的基因 、 、 、 、 和炎症基因 、 、 和 在体外和体内的表达。进一步的研究表明，过表达或激活（罗格列酮）减轻了 TCS 引起的细胞活力、迁移、血管生成抑制和炎症反应，而 PPARγ 的敲低或抑制（GW9662）则产生相反的效果。此外，TCS 导致胎盘功能障碍，表现为胎盘和胎儿的重量和大小明显减少，而 PPARγ 激动剂罗格列酮减轻了小鼠的这种损伤。总之，我们的研究结果表明 TCS 诱导的胎盘功能障碍是通过 PPARγ 通路介导的。我们的研究结果表明，激活 PPARγ 可能是对抗 TCS 暴露对胎盘和胎儿的不良影响的一种有前途的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/d5925c6e2442/cells-11-00086-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/4cd62de2cdb8/cells-11-00086-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/d45556606841/cells-11-00086-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/fce1033d82b3/cells-11-00086-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/30e649611afa/cells-11-00086-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/5e126b99f9e8/cells-11-00086-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/1cf0d63ce380/cells-11-00086-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/1d2ac4b042d3/cells-11-00086-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/d5925c6e2442/cells-11-00086-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/4cd62de2cdb8/cells-11-00086-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/d45556606841/cells-11-00086-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/fce1033d82b3/cells-11-00086-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/30e649611afa/cells-11-00086-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/5e126b99f9e8/cells-11-00086-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/1cf0d63ce380/cells-11-00086-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/1d2ac4b042d3/cells-11-00086-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4996/8750171/d5925c6e2442/cells-11-00086-g008.jpg

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