4.7 Article

Protective Effects of Taraxasterol against Deoxynivalenol-Induced Damage to Bovine Mammary Epithelial Cells

Journal

TOXINS
Volume 14, Issue 3, Pages -

Publisher

MDPI
DOI: 10.3390/toxins14030211

Keywords

taraxasterol; deoxynivalenol; endoplasmic reticulum stress; apoptosis; bovine mammary epithelial cells

Funding

  1. National Natural Science Foundation of China [U21A20251]
  2. Science and Technology Development Program of Jilin Province [20210202039NC]
  3. Jilin Province Technology Extension Project of Improvement Quality and Efficiency of Animal Agriculture [202202]
  4. Changchun City Technology Extension Project of Antibiotic-free livestock and poultry Production [20200000003]
  5. Jilin University Student Innovation and Entrepreneurship Training Program [S202110183624]

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In this study, it was found that taraxasterol can protect bovine mammary epithelial cells from damage caused by deoxynivalenol (DON), reduce cell apoptosis, alleviate endoplasmic reticulum stress, and reduce reactive oxygen species accumulation.
Deoxynivalenol (DON), a mycotoxin produced by Fusarium graminearum, is one of the most prevalent contaminants in livestock feed and causes very large losses to animal husbandry every year. Taraxasterol, isolated from Taraxacum officinale, has anti-inflammatory, antioxidative stress, and antitumor effects. In the present study, bovine mammary epithelial cells (MAC-T) were used as a model, and different concentrations of taraxasterol (0, 1, 5, 10, and 20 mu g/mL) were used to protect against DON-induced cell damage. The results showed that taraxasterol at a concentration of 10 mu g/mL significantly increased cell viability. Analysis of lactate dehydrogenase (LDH) levels indicated that taraxasterol substantially decreased LDH release caused by DON. Taraxasterol effectively alleviated the depletion of glutathione (GSH), the increase in the lipid peroxidation of malondialdehyde (MDA), the reduction in total superoxide dismutase (T-SOD) activity, and the decrease in total antioxidant capacity (T-AOC) induced by DON. The results further showed that taraxasterol reduced the accumulation of reactive oxygen species (ROS). Taraxasterol was found to relieve endoplasmic reticulum (ER) stress by suppressing the expression of glucose-regulated protein 78 kDa (GRP78), activating transcription factor 6 (ATF6), activating transcription factor 4 (ATF4) and the transcription factor C/EBP homologous protein (CHOP), and reducing cell apoptosis by suppressing the expression of caspase-3 and Bcl2-associated X (BAX) and upregulating the expression of the antiapoptotic protein B-cell lymphoma-2 (Bcl-2). Our research results indicate that taraxasterol could alleviate DON-induced damage to MAC-T cells.

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