漏芦通过TLR4/NF-κB通路抑制脂多糖诱导的 小鼠乳腺上皮细胞炎症反应.

In order to explore the anti-inflammatory effect and mechanism of RUEE on LPS-induced mouse mammary epithelial cells (HC11 cells), HC11 cells were treated with RUEE (80 μg/mL), LPS (1 μg/mL) and RUEE (80 μg/mL)+LPS (1 μg/mL) co-treatment. The mRNA expression level of inflammatory cytokines and TLR4 were detected by fluorescence quantitative PCR, and the protein expression of key factors of NF-κB pathway were detected by Western blotting. The results showed that LPS induction could significantly increase the mRNA expression level of TNF-α, COX-2, IL-6, and IL-1β in HC11 cells (P<0.05), obviously up-regulate TLR4 mRNA expression and the phosphorylation level of NF- κB p65 and IκBα (P<0.05). RUEE pretreatment could dramatically reduce the mRNA expression of TNF-α, COX-2, IL-6, and IL-1β in HC11 cells induced by LPS (P<0.05), evidently down-regulate TLR4 mRNA expression and the phosphorylation level of NF-κB p65 and IκBα (P<0.05). It shows that RUEE can inhibit the activation of TLR4/NF-κB pathway to downregulate the overexpression of related inflammatory cytokines and alleviate the LPS-induced inflammatory response of mammary epithelial cells. [ABSTRACT FROM AUTHOR]