DON induced DNA damage triggers absence of p53-mediated G2 arrest and apoptosis in IPEC-1 cells

Hou, Silu; Ma, Jingjiao; Cheng, Yuqiang; Wang, Zhaofei; Wang, Guiping; Jia, Aiqing; Wang, Hengan; Sun, Jianhe; Yan, Yaxian

doi:10.1016/j.tox.2023.153707

Cited by 3 publications

References 46 publications

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Milk‐derived exosomes in the regulation of nutritional and immune functions

Yang,

Wuren,

Zhai

et al. 2024

Food Science & Nutrition

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Milk‐derived exosomes (MDEs), being a component of milk, have the potential to support immune system maturation in offspring and enhance immune cell proliferation. Through the transport and transmission of essential signaling molecules, MDEs contribute to the regulation of intergenerational and intraspecies communication, thereby impacting nutrient uptake and metabolic functions. A comprehensive comprehension of MDE functionalities is imperative for enhancing the quality of the dairy industry. A systematic search of the databases PubMed/Medline, Web of Science, and Scopus utilizing predetermined keywords resulted in the identification of 418 articles, of which 67 were chosen for inclusion in this review, which specifically explores the intersection of immune response and nutrition. This article provides a critical analysis of the classification of extracellular vesicles, the mechanisms underlying the biosynthesis of microvesicular dietary exosomes (MDEs), the components of MDEs, and their relevance in the contexts of nutrition and immune modulation. The primary aim of this review was to offer valuable scholarly insights to support the advancement and practical application of MDEs.

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Milk‐derived exosomes in the regulation of nutritional and immune functions

Yang,

Wuren,

Zhai

et al. 2024

Food Science & Nutrition

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Omics analysis revealed the intestinal toxicity induced by aflatoxin B1 and aflatoxin M1

Gao,

Wang,

et al. 2024

Ecotoxicology and Environmental Safety

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Prodelphinidin from Purple Sweet Potato Induces Apoptosis in Human Triple-Negative Breast Cancer Cells via Reactive Oxygen Species and Endoplasmic Reticulum Stress Through the Mitochondrial Apoptosis Pathways

Zhang,

Chen,

Wang

et al. 2025

Preprint

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Triple negative breast cancer (TNBC), a highly aggressive and heterogeneous subtype of breast cancer, lacks an effective targeted therapy. Conventional medication has limited efficacy in treating TNBC, which highlights the potential of developing therapeutic agents from natural bioactive compounds. This study aimed to investigate the cytotoxicity of prodelphinidin (PD), an anthocyanin found in purple sweet potato, in human MDA-MB-231 and MDA-MB-436 cells. The results showed that PD selectively inhibited human breast cancer, particularly TNBC. Furthermore, PD demonstrated significant dose- and time-dependent inhibition of MDA-MB-231 and MDA-MB-436 cell activity. Flow cytometry and western blot analysis revealed that PD induced cell apoptosis by down-regulating Bcl-2, activating caspase-3/9, and cleaving PARP. Additionally, PD treatment upregulated the expression of p-elF2α, GRP78, and CHOP, indicating the involvement of endoplasmic reticulum stress (ERS). PD treatment also increased the production of reactive oxygen species (ROS) and decreased superoxide dismutase（SOD）activity in TNBC cells. The cytotoxicity of PD reduced significantly by pre-treatment with caspase inhibitors (Ac-DEVD-CHO and Z-LEHD-FMK). In conclusion, PD effectively inhibited the proliferation and induced apoptosis in TNBC cells through the activation of ROS and endoplasmic reticulum stress.

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DON induced DNA damage triggers absence of p53-mediated G2 arrest and apoptosis in IPEC-1 cells

Cited by 3 publications

References 46 publications

Milk‐derived exosomes in the regulation of nutritional and immune functions

Milk‐derived exosomes in the regulation of nutritional and immune functions

Omics analysis revealed the intestinal toxicity induced by aflatoxin B1 and aflatoxin M1

Prodelphinidin from Purple Sweet Potato Induces Apoptosis in Human Triple-Negative Breast Cancer Cells via Reactive Oxygen Species and Endoplasmic Reticulum Stress Through the Mitochondrial Apoptosis Pathways

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