# Apricot Bee Pollen Alleviates Deoxynivalenol-Induced Cellular Toxicity in Bovine Granulosa Cells

## TL;DR

Apricot bee pollen helps protect cow egg-supporting cells from damage caused by a harmful fungus toxin, suggesting it could be a natural way to prevent reproductive issues.

## Contribution

Apricot bee pollen ethanol extract is shown to mitigate deoxynivalenol-induced toxicity in bovine granulosa cells through antioxidant and estrogen-regulating effects.

## Key findings

- Deoxynivalenol induces apoptosis, estrogen dysfunction, and oxidative stress in bovine granulosa cells.
- Apricot bee pollen ethanol extract restores cell viability and estrogen balance while reducing oxidative stress.
- ABPE upregulates antioxidant gene HO-1 and counteracts DON-induced ROS and MDA increases.

## Abstract

In the present study, we explored the toxic effects and mechanisms of deoxynivalenol exposure in bovine granulosa cells, and observed that deoxynivalenol could induce apoptosis, estrogen dysfunction, and oxidative stress by increasing the levels of reactive oxygen species and malondialdehyde. Importantly, apricot bee pollen ethanol extract was found to mitigate the reduction in cell viability, restore estrogen balance, and alleviate oxidative stress in bovine granulosa cells induced by deoxynivalenol. Our study provides new insights regarding the protective effects of bee pollen against cellular toxicity induced by deoxynivalenol, suggesting that bee pollen is a promising natural agent for preventing reproductive toxicity caused by mycotoxin contamination.

Apricot bee pollen is an important natural product that exhibits antioxidant, anti-inflammatory, and antimicrobial properties. Deoxynivalenol (DON), one of the most prevalent mycotoxins produced by Fusarium fungi, poses risks to both human and animal reproductive systems. We observed that exposure to DON inhibited cell proliferation and induced apoptosis in bovine granulosa cells (bGCs), accompanied by a significant downregulation of PCNA expression and an upregulation of BAX expression. RNA sequencing analysis revealed that differentially expressed genes (DEGs) were primarily enriched in the oxidation-reduction process, oxidoreductase activity, and steroid biosynthesis. We further confirmed that DON exposure inhibited the production of estrogen and progesterone by decreasing the protein expression levels of CYP19A1 and StAR. Additionally, DON exposure increased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in a dose-dependent manner, suggesting that DON induced oxidative stress in bGCs. Importantly, we demonstrated that apricot bee pollen ethanol extract (ABPE) increased the cell viability of bGCs and alleviated the effects of DON-induced cell viability reduction and estrogen dysfunction. Furthermore, ABPE attenuated the DON-induced increase in ROS levels and upregulated the expression of antioxidant-related gene heme oxygenase-1 (HO-1). These results reveal the protective effects of ABPE against DON-induced cell viability reduction, estrogen disorder, and oxidative stress, providing new insights into the potential of bee pollen as a promising natural agent to improve mycotoxin contamination.