Dimethyl itaconate protects against lippolysacchride-induced mastitis in mice by activating MAPKs and Nrf2 and inhibiting NF-κB signaling pathways

The aim of this study is to investigate the protective role of dimethyl itaconate -the membranepermeable derivative of itaconate, on LPS-induced mastitis in mice

Caijun Zhao; Peng Jiang; Zhaoqi He; Xin Yuan; Jian Guo; Yanyi Li; Xiaoyu Hu; Yongguo Cao; Yunhe Fu; Naisheng Zhang


Scholarcy highlights

  • As the main disease to affect the dry dairy cow with the characterized by increasing number of somatic cells in milk and reducing milk production, has been known as one of the most serious expensive disease for the dairy industry
  • To establish the model of mastitis, mice 5–7 day after delivery were utilized by nipple duct injection of LPS, while dimethyl itaconate was treated 24h intraperitoneally before LPS injection
  • To clarify the underling mechanisms of the protective role of DI on mastitis, the MAPKs, NF-κB and Nrf2 signaling pathways were detected via western blotting
  • The results demonstrated that DI markedly decreased the pathological injury of mammary, and considerably reduced the production of TNF-α and IL-1β, as well as up-regulated the Nrf2, HO-1, phosphorylation of p38 and ERK, but down-regulated TLR4 and phosphorylation of p65 NF-κB
  • Our research recommended that DI ameliorated LPS-induced mastitis which highlights itaconate may as a potential candidate to protect against mastitis

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