| Summary: | 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 (<i>p</i> < 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 (<i>p</i> < 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.
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