This experiment evaluated the pre-protective effect of AAE on inflammatory injury and tight junction disturbance in bMECs induced by LPS. The bMECs were treated with AAE (3, 6, 12 μg/mL) for 3 h and then incubated with 10 μg/mL lipopolysaccharide (LPS) for 12 h. Our results showed that LPS significantly increased the mRNA and protein expression of CD36, induced the phosphorylation of IκBα and p65 and elevated the levels of TNF-α, IL-1β and IL-6 mRNA, which further resulted in ultrastructural damage, disrupted the expression of tight junction proteins (occludin, zonula occludens (ZO-1) and claudin-1) and decreased the viability of bMECs (p < 0.05). More importantly, AAE pretreatment attenuated the expression of CD36, suppressed the activity of the NF-κB signaling pathway and down-regulated the levels of inflammatory factors in LPS-stimulated bMECs (p < 0.05). Therefore, AAE can effectively protect bMECs against inflammatory injury and tight junction dysfunction, which has important research value for the prevention of bovine mastitis.

Mastitis is recognized worldwide as one of the most expensive and common bovine diseases, severely affecting bovine health and milk quality. Mitochondria, known to play important roles in bovine mammary epithelial cells (BMECs), not only provide energy for milk synthesis but also participate in the regulation of the intracellular redox balance, inflammatory reactions, calcium signal transduction, and apoptosis. Mastitis destroys the dynamic balance between the intrinsic repair and damage mechanisms of mitochondria, which leads to mitochondrial dysfunction and aggravation of mammary cell injury or apoptosis. Plant extracts are rich in bioactive substances and are promising antibiotic substitutes for alleviating bovine mastitis. This paper reviews the mechanism through which plant extracts promote mitochondrial repair by interfering with mitophagy, dynamic balance and biogenesis, and alleviate mitochondrial damage by inhibiting mitochondrial ROS, calcium homeostasis imbalance and permeability changes, resulting in the regulation of the mitochondrial function of mammary cells under inflammation and oxidative stress. Elucidation of these mechanisms can provide new strategies for the targeted control of bovine mastitis.