Absorption and Transport Mechanism of Red Meat-Derived N-glycolylneuraminic Acid and Its Damage to Intestinal Barrier Function through the NF-κB Signaling Pathway
He E, Quan W, Luo J, Liu C, Zheng W, Shen Q
Toxins · 6 citas
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- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Natural Science Foundation of China
- Gobierno
- National Nature Science Foundation of China
- Subvenciones
- National Natural Science Foundation of China (31771992)
Según 2 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2023-02-06 · Toxins (Basel) · vol. 15 · número 2 · pág. 132
- Editorial
- Multidisciplinary Digital Publishing Institute
- Citado
- 12 citas · más que el 76% de estudios similares · 1.1× el promedio de su campo
- Referencias
- 45 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Barrier Structure and Function Studies · Gut microbiota and health · Cancer-related molecular mechanisms research
- Palabras clave
- Endocytosis, Cell biology, Exocytosis, Brefeldin A, Occludin, Cytochalasin D, Biology, Endocytic cycle, Chemistry, Biochemistry, Tight junction, Secretion, Cytoskeleton, Golgi apparatus, Cell
- MeSH
- intestinal mucosa, caco-2 cells, humans, neuraminic acids, hydrazones, brefeldin a, nystatin, monensin, chlorpromazine, nf-kappa b, signal transduction, claudin-1, occludin
6 autores
- Enqi He🇨🇳Hunan Agricultural University
- Wei Quan🇨🇳Hunan Agricultural University
- Jie Luo🇨🇳Hunan Agricultural University
- Chuxin Liu🇨🇳Hunan Agricultural University
- Wanting Zheng🇨🇳Hunan Agricultural University
- Qingwu W. Shen🇨🇳 · autor de correspondenciaHunan Agricultural University
Resumen
El texto original del estudio, en el idioma en que se publicó.
N-glycolylneuraminic acid (Neu5Gc) is a specific factor in red meat that induces intestinal disease. Our aim was to investigate the effect of Neu5Gc on the intestinal barrier as well as its mechanism of endocytosis and exocytosis. Ten specific inhibitors were used to explore the mechanism of Neu5Gc endocytosis and exocytosis by Caco-2 cells. Amiloride hydrochloride and cytochalasin D had the strongest inhibitory effect on the endocytosis of Neu5Gc. Sodium azide, dynasore, chlorpromazine hydrochloride, and nystatin also inhibited Neu5Gc endocytosis. Dynasore exhibited a stronger inhibitory effect than that of chlorpromazine hydrochloride or nystatin alone. Exocytosis inhibitors, including nocodazole, brefeldin A, monensin, and bafilomycin A, inhibited the transmembrane transport of Neu5Gc. Monensin promoted the exocytosis of Neu5Gc from Caco-2 cells. In another experiment, we observed no significant inhibitory effects of monensin and brefeldin A. Dietary concentrations of Neu5Gc induced prominent damage to intestinal tight junction proteins zonula occludens-1 (ZO-1), occludin, and claudin-1 and promoted the phosphorylation of IκB-α and P65 to activate the canonical Nuclear Factor kappa-B (NF-κB) pathway. Neu5Gc increased the RNA levels of pro-inflammatory factors IL-1β, IL-6, and TNF-α and inhibited those of anti-inflammatory factors TGF-β and IL-10. BAY, an NF-κB signaling pathway inhibitor, attenuated these changes. Reductions in the levels of ZO-1, occludin, and claudin-1 were recovered in response to BAY. Our data reveal the endocytosis and exocytosis mechanism of Neu5Gc and prove that Neu5Gc can activate the canonical NF-κB signaling pathway, regulate the transcription of inflammatory factors, thereby damaging intestinal barrier function.
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