Effects of Maillard-type caseinate glycation on the preventive action of caseinate digests in acrylamide-induced intestinal barrier dysfunction in IEC-6 cells.
Jia ShiYu FuXin-Huai ZhaoPublished in: RSC advances (2018)
Dietary acrylamide has attracted widespread concern due to its toxic effects; however, its adverse impact on the intestines is less assessed. Protein glycation of the Maillard-type is widely used for property modification, but its potential effect on preventive efficacy of protein digest against the acrylamide-induced intestinal barrier dysfunction is quite unknown. Caseinate was thus glycated with lactose. Two tryptic digests from the glycated caseinate and untreated caseinate (namely GCN digest and CN digest) were then assessed for their protective effects against acrylamide-induced intestinal barrier dysfunction in the IEC-6 cell model. The results showed that acrylamide at 1.25-10 mmol L -1 dose-dependently had cytotoxic effects on IEC-6 cells, leading to decreased cell viability and increased lactate dehydrogenase release. Acrylamide also brought about barrier dysfunction, including decreased trans-epithelial electrical resistance (TEER) value and increased epithelial permeability. However, the two digests at 12.5-100 μg mL -1 could alleviate this dysfunction via enhancing cell viability by 70.2-83.9%, partly restoring TEER values, and decreasing epithelial permeability from 100% to 76.6-94.1%. The two digests at 25 μg mL -1 strengthened the tight junctions via increasing tight junction proteins ZO-1, occludin, and claudin-1 expression by 11.5-68.6%. However, the results also suggested that the GCN digest always showed lower protective efficacy than the CN digest in the cells. It is concluded that Maillard-type caseinate glycation with lactose endows the resultant tryptic digest with impaired preventive effect against acrylamide-induced intestinal barrier dysfunction, highlighting another adverse effect of the Maillard reaction on food proteins.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- high glucose
- cell cycle arrest
- drug induced
- blood brain barrier
- squamous cell carcinoma
- signaling pathway
- cell death
- poor prognosis
- stem cells
- cell proliferation
- emergency department
- binding protein
- endoplasmic reticulum stress
- risk assessment
- lymph node metastasis
- single molecule
- climate change
- pi k akt