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

Abstract

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 μg/mL) were used to protect against DON-induced cell damage. The results showed that taraxasterol at a concentration of 10 μg/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.

Keywords

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