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Lauric acid alleviates deoxynivalenol-induced intestinal stem cell damage by potentiating the Akt/mTORC1/S6K1 signaling axis
- Source :
- Chemico-biological interactions. 348
- Publication Year :
- 2021
-
Abstract
- Intestinal stem cell (ISC)-driven intestinal homeostasis is subjected to dual regulation by dietary nutrients and toxins. Our study investigated the use of lauric acid (LA) to alleviate deoxynivalenol (DON)-induced intestinal epithelial damage. C57BL/6 mice in the control, LA, DON, and LA + DON groups were orally administered PBS, 10 mg/kg BW LA, 2 mg/kg BW DON, and 10 mg/kg BW LA + 2 mg/kg BW DON for 10 days. The results showed that LA increased the average daily gain and average daily feed intake of the mice exposed to DON. Moreover, the DON-triggered impairment of jejunal morphology and barrier function was significantly improved after LA supplementation. Moreover, LA rescued ISC proliferation, inhibited intestinal cell apoptosis, and promoted ISC differentiation into absorptive cells, goblet cells, and Paneth cells. The jejunum crypt cells from the mice in the LA group expanded into enteroids, resulting in a significantly greater enteroid area than that in the DON group. Furthermore, LA reversed the DON-mediated inhibition of the Akt/mTORC1/S6K1 signaling axis in the jejunum. Our results indicated that LA accelerates ISC regeneration to repair intestinal epithelial damage after DON insult by reactivating the Akt/mTORC1/S6K1 signaling pathway, which provides new implications for the function of LA in ISCs.
- Subjects :
- Male
medicine.medical_specialty
Crypt
P70-S6 Kinase 1
Apoptosis
mTORC1
Mechanistic Target of Rapamycin Complex 1
Toxicology
digestive system
Ribosomal Protein S6 Kinases, 90-kDa
Jejunum
Mice
Internal medicine
medicine
Animals
Protein kinase B
Barrier function
Cell Proliferation
Chemistry
Stem Cells
Lauric Acids
Cell Differentiation
General Medicine
Intestines
Mice, Inbred C57BL
Endocrinology
medicine.anatomical_structure
Stem cell
Trichothecenes
Proto-Oncogene Proteins c-akt
Signal Transduction
Subjects
Details
- ISSN :
- 18727786
- Volume :
- 348
- Database :
- OpenAIRE
- Journal :
- Chemico-biological interactions
- Accession number :
- edsair.doi.dedup.....956eee4a04e3117b6ef9c7f920ab4f5b