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The intestine serves mainly as a place for digestion and absorption and functions as an immune
and endocrine organ. Intestinal stem cells (ISCs) play critical roles in the maintenance of intestinal homeostasis
and regeneration, and a complex of signaling pathways is involved in these processes. The
Notch signaling pathway is induced via distinct cell-to-cell connections, which are activated through the
binding of the Notch ligand on the surface of niche cells to the Notch receptor on ISCs. Numerous studies
have shown the central importance of Notch signaling in the proliferation and differentiation of ISCs.
Here, we summarize the latest research progress on the crucial functions of Notch signaling in maintaining
homeostasis and determining the cell fate of ISCs. Furthermore, the challenges of Notch signaling in
colon cancer therapy strategies are also discussed. Several important questions regarding Notch regulation
of ISCs are proposed.
Deoxynivalenol (DON) is a threatening mycotoxin primarily present in the agricultural environment, especially in food commodities and animal forages, and exerts significant global health hazards. Lycopene (LYC) is a potent antioxidant carotenoid mainly present in tomatoes and other fruits with enormous health benefits. The present study was designed to ascertain whether LYC could protect DON-induced intestinal epithelium oxidative injury by regulating Keap1/Nrf2 signaling in the intestine of mice. A total of forty-eight mice were randomly distributed into four groups (n = 12), Control (CON), 10 mg/kg BW LYC, 3 mg/kg BW DON, and 3 mg/kg DON + 10 mg/kg LYC BW (DON + LYC). The experimental groups were treated by intragastric administration for 11 days. Our results showed that LYC significantly increased average daily feed intake (ADFI), average daily gain (ADG), and repaired intestinal injury and barrier dysfunction, as evident by increased trans-epithelial electrical resistance (TEER) and decreased diamine oxidase (DAO) activity, as well as up-regulated tight junction proteins (occludin, claudin-1) under DON exposure. Furthermore, LYC treatment stabilized the functions of intestinal epithelial cells (Lgr5, PCNA, MUC2, LYZ, and Villin) under DON exposure. Additionally, LYC alleviated DON-induced oxidative stress by reducing ROS and MDA accumulation and enhancing the activity of antioxidant enzymes (CAT, T-SOD, T-AOC, and GSH-Px), which was linked with the activation of Nrf2 signaling and degradation of Keap1 expression. Conclusively, our findings demonstrated that LYC protects intestinal epithelium from oxidative injury by modulating the Keap1/Nrf2 signaling pathway under DON exposure. These novel findings could lead to future research into the therapeutic use of LYC to protect the DON-induced harmful effects in humans and/or animals.
The small intestinal epithelium is regulated in response
to various
beneficial or harmful environmental information. Deoxynivalenol (DON),
a mycotoxin widely distributed in cereal-based feeds, induces oxidative
stress damage in the intestine due to the mitochondrial stress. As
a functional nutrient, selenomethionine (Se-Met) is involved in synthesizing
several antioxidant enzymes, yet whether it can replenish the intestinal
epithelium upon DON exposure remains unknown. Therefore, the in vivo model C57BL/6 mice and the in vitro model MODE-K cells were treated with l-Se-Met and DON alone
or in combination to confirm the status of intestinal stem cell (ISC)-driven
epithelial regeneration. The results showed that 0.1 mg/kg body weight
(BW) Se-Met reinstated the growth performance and integrity of jejunal
structure and barrier function in DON-challenged mice. Moreover, Lgr5+ ISCs and PCNA+ mitotic cells in crypts were prominently
increased by Se-Met in the presence of DON, concomitant with a significant
increase in absorptive cells, goblet cells, and Paneth cells. Simultaneously,
crypt-derived jejunal organoids from the Se-Met + DON group exhibited
more significant growth advantages ex vivo. Furthermore,
Se-Met-stimulated Keap1/Nrf2-dependent antioxidant system (T-AOC and
GSH-Px) to inhibit the accumulation of ROS and MDA in the jejunum
and serum. Moreover, Se-Met failed to rescue the DON-triggered impairment
of cell antioxidant function after Nrf2 perturbation using its specific
inhibitor ML385 in MODE-K cells. In conclusion, Se-Met protects ISC-driven
intestinal epithelial integrity against DON-induced oxidative stress
damage by modulating Keap1/Nrf2 signaling.
Sex identification plays an important role in avian production. Hitherto, it is difficult to distinguish the sexes of monomorphic birds based on their external features. The chromo-helicase-DNA-binding genes contain CHD-W gene and CHD-Z gene, which are located on the W chromosome and Z chromosome, respectively. Since CHD-W gene is unique to females, the polymerase chain reaction can be used for sex identification. However, extracting DNA procedures for verifying the sex is tedious and expensive. To address these disadvantages, the objective of this study was to develop a simple DNA extraction assay to efficiently process blood, liver, and feather samples. The results showed that 2% dimethylsulfoxide was suitable for processing blood, and phosphate-buffered saline was suitable for processing liver and feather samples. The specific primers were designed, and the length of the targets is 474 bp on Z chromosome and 319 bp on W chromosome. The pigeons were identified as females based on the presence of two bands on the gel, and as males based on the presence of one band. Taken together, our results suggested that feather samples were more appropriate than blood or liver for sex identification of pigeons. Compared to the traditional DNA extraction, this method shortened the assay time and reduced the cost.
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