Palmatine Attenuates LPS-Induced EMT in MAC-T Cells and Mammary Fibrosis in Mice, with Suppression of NF-κB/TGF-β1/Smad Signaling In Vivo

巴马汀通过抑制体内NF-κB/TGF-β1/Smad信号通路,减弱LPS诱导的MAC-T细胞EMT和小鼠乳腺纤维化。

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Abstract

Bovine mastitis is a common inflammatory disease that can progress to mammary fibrosis, thereby impairing udder health, milk yield, and milk quality. This study investigated the protective effects of palmatine on lipopolysaccharide (LPS)-induced epithelial–mesenchymal transition (EMT) in bovine mammary epithelial cells and mammary fibrosis in mice, as well as the underlying mechanisms. In vitro, palmatine markedly reversed LPS-induced EMT by increasing E-cadherin expression and decreasing N-cadherin and α-SMA expression. In vivo, palmatine alleviated inflammatory cell infiltration and collagen deposition in mammary tissue and reduced the expression of TGF-β1, p-Smad2, p-Smad3, p-p65, TNF-α, IL-1β, and IL-6. These findings suggest that palmatine alleviates LPS-induced mammary fibrosis, possibly through inhibition of the NF-κB/TGF-β1/Smad signaling pathway, and may represent a potential therapeutic strategy for the prevention and treatment of mammary fibrosis.

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