Palmatine has a wide range of pharmacological effects and anti‐inflammatory function. However, the effect of palmatine on LPS‐induced inflammatory response of mammary epithelial cells has not been reported. In this research, we studied the anti‐inflammatory mechanism of palmatine in EpH4‐Ev (mouse mammary epithelial cells). EpH4‐Ev cells were pre‐treated with palmatine and then incubated with LPS. Cells were collected for examining production of pro‐inflammatory mediators by qRT‐PCR, and the related inflammatory signalling pathway was detected through immunofluorescence and Western blot. The results found that palmatine could significantly reduce the expression of IL‐6, TNF‐α, IL‐1β and COX‐2 in EpH4‐Ev cells. Research on mechanisms found that palmatine could significantly inhibit the protein levels of p‐Akt, p‐P65, p‐ERK1/2 and p‐P38 in EpH4‐Ev cells. In conclusion, these data suggested that palmatine inhibits inflammatory response in LPS‐induced EpH4‐Ev cells via down‐regulating Akt/ NF‐кB, ERK1/2 and P38 signalling pathways.

中文翻译：

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Palmatine 通过抑制 ERK1/2、P38 和 Akt/NF-кB 信号通路减弱 LPS 诱导的小鼠乳腺上皮细胞炎症反应。

巴马汀具有广泛的药理作用和抗炎作用。然而，巴马汀对 LPS 诱导的乳腺上皮细胞炎症反应的影响尚未见报道。在这项研究中，我们研究了巴马汀在 EpH4-Ev（小鼠乳腺上皮细胞）中的抗炎机制。EpH4-Ev 细胞用巴马汀预处理，然后用 LPS 孵育。收集细胞以通过 qRT-PCR 检查促炎介质的产生，并通过免疫荧光和蛋白质印迹检测相关的炎症信号通路。结果发现巴马汀可显着降低IL-6、TNF-α、IL-1β和COX-2的表达在 EpH4-Ev 细胞中。机制研究发现，巴马汀可显着抑制 EpH4-Ev 细胞中 p-Akt、p-P65、p-ERK1/2 和 p-P38 的蛋​​白水平。总之，这些数据表明巴马汀通过下调 Akt/NF-кB、ERK1/2 和 P38 信号通路抑制 LPS 诱导的 EpH4-Ev 细胞的炎症反应。