Deoxynivalenol exposure disturbs the cytoplasmic maturation in porcine oocytes DOI Creative Commons

Linlin Hu,

Yaxi Liu, Xiaoting Yu

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 285, С. 117137 - 117137

Опубликована: Сен. 30, 2024

Язык: Английский

Luteolin Inhibits Dexamethasone‐Induced Osteoporosis by Autophagy Activation Through miR‐125b‐5p/SIRT3/AMPK/mTOR Axis, an In Vitro and In Vivo Study DOI Creative Commons
Liang Tang, Xinyu Fan, Yongqing Xu

и другие.

Food Science & Nutrition, Год журнала: 2025, Номер 13(3)

Опубликована: Март 1, 2025

ABSTRACT Luteolin (LUT) has been suggested as an inhibitor of osteoporosis (OP). This investigation examines the pivotal role miR‐125b‐5p/SIRT3/AMPK/mTOR pathway in mediating luteolin‐induced effects on OP. Mesenchymal stem cells derived from bone marrow (BMSCs) were exposed to dexamethasone (DEX) create vitro model Following treatment with luteolin, levels miR‐125b‐5p and SIRT3 quantified using reverse transcription polymerase chain reaction. Moreover, SIRT3, AMPK, mTOR protein levels, osteogenesis (OPN, Runx2, OSX, OCN), autophagy (p62, ATG5, LC3, BECN1) evaluated ELISA. Additionally, specific mimics siRNA constructed overexpress or downregulate SIRT3. Furthermore, animal models DEX‐induced OP assess LUT at doses 50 100 mg/kg/day histology, stereology, biochemistry, expression miR‐125b‐5p, SIRT3/AMPK/mTOR axis, markers autophagy. The findings revealed that suppressed expression, overexpressed downregulated BMSCs compared DEX ( p ‐value < 0.01). Interestingly, restored for 0.001). overexpression downregulation inhibited therapeutic properties. In animals, improved histology 0.05) while overexpressing AMPK RUNX2, OPN, OCN improved, was enhanced LUT‐treated rats. current could promote improve via activation through pathway.

Язык: Английский

Процитировано

0

Natural Phenolic Compounds against Trichothecenes: From Protective Mechanisms to Future Perspectives DOI
Aimei Liu, Kan Zhu,

Chenchen Song

и другие.

Journal of Agricultural and Food Chemistry, Год журнала: 2025, Номер unknown

Опубликована: Апрель 2, 2025

Trichothecenes (TCNs), Fusarium-derived mycotoxins exemplified by deoxynivalenol and T-2 toxin, threaten global health through multisystem toxicity widespread contamination. Natural phenolic compounds (NPCs), leveraging their intrinsic safety natural abundance, demonstrate multimechanistic efficacy in counteracting TCN toxicity. This article reviews both domestic international research on the protective mechanisms of NPCs against TCN-induced exert effects multitiered mechanisms: (1) molecular regulation via Nrf2-centric antioxidant activation MAPK/NF-κB inflammatory axis suppression, coupled with coordinated inhibition programmed cell death pathways (apoptosis/ferroptosis/pyroptosis) autophagy modulation, where GPX4 emerges as a critical ferroptosis regulator; (2) restoring microbiome balance, enhancing intestinal barrier function, optimizing nutrient transport. Gut microflora may also serve an additional target for mitigating TCNs. further inhibit Fusarium proliferation mycotoxin biosynthesis. While there is demonstrated potential food sustainable feed development, challenges persist bioavailability optimization, pharmacokinetic profiling, microbiota-metabolite crosstalk. analysis advances NPC-based strategies detoxification agriculture.

Язык: Английский

Процитировано

0

Peroxiredoxin 4 Ameliorates T-2 Toxin-Induced Growth Retardation in GH3 Cells by Inhibiting Oxidative Stress and Apoptosis DOI Creative Commons
Qirong Lu, Yi Zhu,

Luyao Wang

и другие.

Molecules, Год журнала: 2024, Номер 29(23), С. 5491 - 5491

Опубликована: Ноя. 21, 2024

T-2 toxin, a highly toxic type A trichothecene, is secondary fungal metabolite produced by various Fusarium species. The consumption of food and feed contaminated with toxin major factor contributing to growth retardation, posing significant risks both human animal health. However, the specific targets mechanisms that mitigate toxin-induced retardation remain unclear. In this study, transcriptomic analysis was employed identify key differentially expressed genes associated alleviation retardation. Peroxiredoxin 4 (PRDX4), gene linked oxidative stress apoptosis, found be one most downregulated in toxin-treated GH3 cells, an vitro model experiments demonstrated significantly increased reactive oxygen species' production, cell cycle arrest while reducing activity antioxidant enzymes (superoxide dismutase glutathione peroxidase) PRDX4 expression cells. Furthermore, silencing exacerbated whereas overexpression effectively mitigated these effects. These findings highlight protective role counteracting suggesting can serve as therapeutic target for treatment

Язык: Английский

Процитировано

2

Deoxynivalenol exposure disturbs the cytoplasmic maturation in porcine oocytes DOI Creative Commons

Linlin Hu,

Yaxi Liu, Xiaoting Yu

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 285, С. 117137 - 117137

Опубликована: Сен. 30, 2024

Язык: Английский

Процитировано

1