Bisphenol A inhibits mucin 2 secretion in intestinal goblet cells through mitochondrial dysfunction and oxidative stress - 16/02/19
, Wei Qu b, 1 , Kai Wang c, 1 , Sijin Chen d , Lijin Zhang e , Danlian Wu b , Zhigao Chen b, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Aims |
Bisphenol A (BPA) can induce intestinal epithelial cell barrier dysfunction; however, its effects on the intestinal mucus barrier remain unclear. We used LS174T cells as a model to investigate the effects of BPA on the functions of intestinal goblet cells.
Main methods |
This study used CCK-8, flow cytometry, ELISA and real-time PCR to investigate the effects of BPA on mitochondrial dynamics, oxidative stress and apoptosis in goblet cells. In addition, mucin synthesis and secretion were evaluated using PAS staining and a PAS assay, respectively.
Key findings |
Our results indicate that BPA reduced cell viability in a time- and concentration-dependent manner. BPA induced mitochondrial dysfunction, as indicated by the depolarization of the mitochondrial membrane potential, inhibition of mitochondrial respiratory chain complex enzyme activity and reduction of ATP production. Moreover, BPA caused oxidative stress by significantly increasing the accumulation of ROS, as well as oxidative stress products, and reducing the antioxidant capacity. Furthermore, BPA induced intestinal goblet cell apoptosis, accompanied by increased DNA fragmentation, caspase-3, -8, -9,-10 gene expression and enzyme activity. Additionally, BPA inhibited the synthesis and secretion of mucin 2.
Significance |
Our data suggest that BPA affected the secretory function of intestinal goblet cells by inducing mitochondrial dysfunction, oxidative stress, and apoptosis.
Le texte complet de cet article est disponible en PDF.Abbreviations : BPA, DMSO, ELISA, H2O2, LD, MDA, MUC, PAS, ROS, SOD, T-AOC
Keywords : Bisphenol A, Mitochondria, Oxidative stress, Mucin, Intestinal goblet cells
Plan
Vol 111
P. 901-908 - mars 2019 Retour au numéro
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