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双酚A和邻苯二甲酸二异丁酯联合暴露通过Notch信号通路和肠道微生物群失调诱导小鼠肠道黏膜屏障损伤

Combined BPA and DIBP Exposure Induced Intestinal Mucosal Barrier Impairment Through the Notch Pathway and Gut Microbiota Dysbiosis in Mice.

作者信息

Duan Mengge, Wang Yuting, Chen Shiyu, Lu Jiawen, Dong Ruihong, Yu Qiang, Xie Jianhua, Chen Yi

机构信息

State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang 330047, China.

出版信息

Foods. 2025 Jan 12;14(2):214. doi: 10.3390/foods14020214.

DOI:10.3390/foods14020214
PMID:39856883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11765467/
Abstract

Bisphenol A (BPA) and diisobutyl (DIBP) phthalate are widely used as typical plasticizers in food packaging. Plasticizers can be released from polymers, migrate into food, and be ingested by humans, leading to various health problems. However, little research has investigated the combined toxicity of BPA and DIBP, particularly their intestinal toxicity. Our goal is to analyse the combined toxicity of BPA (50 mg/kg) and DIBP (500 mg/kg) on the intestines of KM mice. Additionally, we tried to find natural products that can inhibit or prevent the combined toxicity of BPA and DIBP. The results indicated that the combination of BPA and DIBP exposure resulted in a reduction of beneficial flora, an increase in D-Lac levels (136 ± 14 μmol/L), an increase in intestinal permeability, activation of the notch pathway, and a decline in intestinal stem cells (ISCs) to goblet cells, compared to single-exposure sources. Nevertheless, Hu phenolic extract (RHPE) (200, 400 and 600 mg/kg) ameliorated the BPA and DIBP-induced intestinal microbiota disruption and intestinal mucosal barrier impairment by inhibiting the overactivation of the notch pathway. The results of this study highlight the potential risks to human health posed by the combination of BPA and DIBP and may help explain the potential pathways of enterotoxicity caused by combined ingestion.

摘要

双酚A（BPA）和邻苯二甲酸二异丁酯（DIBP）作为典型的增塑剂广泛应用于食品包装中。增塑剂可从聚合物中释放出来，迁移到食品中并被人体摄入，从而导致各种健康问题。然而，很少有研究调查BPA和DIBP的联合毒性，尤其是它们的肠道毒性。我们的目标是分析BPA（50毫克/千克）和DIBP（500毫克/千克）对KM小鼠肠道的联合毒性。此外，我们试图寻找能够抑制或预防BPA和DIBP联合毒性的天然产物。结果表明，与单一暴露源相比，BPA和DIBP联合暴露导致有益菌群减少、D-乳酸水平升高（136±14微摩尔/升）、肠道通透性增加、Notch通路激活以及肠道干细胞（ISC）向杯状细胞的数量下降。然而，胡酚提取物（RHPE）（200、400和600毫克/千克）通过抑制Notch通路的过度激活，改善了BPA和DIBP诱导的肠道微生物群紊乱和肠黏膜屏障损伤。本研究结果突出了BPA和DIBP联合作用对人类健康构成的潜在风险，并可能有助于解释联合摄入导致肠毒性的潜在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/363f8fb64ed3/foods-14-00214-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/0a5f2451d89c/foods-14-00214-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/86d95f383c58/foods-14-00214-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/44f77a224bb1/foods-14-00214-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/45914d93c65d/foods-14-00214-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/d37946b0b845/foods-14-00214-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/f0ec6c36089e/foods-14-00214-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/cb1efba4088e/foods-14-00214-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/ad371e08ec92/foods-14-00214-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/d31a7a783f49/foods-14-00214-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/363f8fb64ed3/foods-14-00214-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/0a5f2451d89c/foods-14-00214-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/86d95f383c58/foods-14-00214-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/44f77a224bb1/foods-14-00214-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/45914d93c65d/foods-14-00214-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/d37946b0b845/foods-14-00214-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/f0ec6c36089e/foods-14-00214-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/cb1efba4088e/foods-14-00214-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/ad371e08ec92/foods-14-00214-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/d31a7a783f49/foods-14-00214-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c4c/11765467/363f8fb64ed3/foods-14-00214-g010.jpg

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[1]
Combined BPA and DIBP Exposure Induced Intestinal Mucosal Barrier Impairment Through the Notch Pathway and Gut Microbiota Dysbiosis in Mice.

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本文引用的文献

[1]
Sub-acute bisphenol A exposure induces proteomic alterations and impairs male reproductive health in mice.

J Biochem Mol Toxicol. 2024-10

[2]
Therapeutic effects and mechanisms of isoxanthohumol on DSS-induced colitis: regulating T cell development, restoring gut microbiota, and improving metabolic disorders.

Inflammopharmacology. 2024-6

[3]
Systemic investigation of di-isobutyl phthalate (DIBP) exposure in the risk of cardiovascular via influencing the gut microbiota arachidonic acid metabolism in obese mice model.

Regen Ther. 2024-4-11

[4]
Exopolysaccharides Produced by subsp. YS108R Ameliorates DSS-Induced Ulcerative Colitis in Mice by Improving the Gut Barrier and Regulating the Gut Microbiota.

J Agric Food Chem. 2024-4-3

[5]
Disruption of intestinal epithelial permeability in the Co-culture system of Caco-2/HT29-MTX cells exposed individually or simultaneously to acrylamide and ochratoxin A.

Food Chem Toxicol. 2024-4

[6]
Forsythia suspensa polyphenols regulate macrophage M1 polarization to alleviate intestinal inflammation in mice.

Phytomedicine. 2024-3

[7]
The impact of dioctyl phthalate exposure on multiple organ systems and gut microbiota in mice.

Heliyon. 2023-11-20

[8]
Research progress of the effects of bisphenol analogues on the intestine and its underlying mechanisms: A review.

Environ Res. 2024-2-15

[9]
antibacterial effects of leaf extract and its anti-colitis in DSS-treated mice.

Front Cell Infect Microbiol. 2023

[10]
Exopolysaccharides from Genistein-Stimulated Ameliorate Cyclophosphamide-Induced Intestinal Injury via PI3K/AKT-MAPKs/NF-κB Pathways and Regulation of Gut Microbiota.

J Agric Food Chem. 2023-9-6

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