Mastitis impairs animal health and results in economic loss. Lipopolysaccharide (LPS) may cause immune response and inflammation in the bovine mammary gland. Hydrogen sulfide (H2S) is the third gasotransmitter that acts as an anti-inflammation regulator in many cells. Despite the importance of H2S in regulating inflammation, the effect and mechanism of exogenous H2S on LPS-induced inflammation in bovine mammary epithelial cells are unknown. In the present study, with NaHS as a donor of H2S, the bovine mammary epithelial cell line (MAC-T) was applied as an in vitro model to study the role of H2S on LPS-induced MAC-T cells. The results verified that the cell viability was diminished by LPS but restored by exogenous H2S at a physiologically relevant concentration (10 μM). Additionally, the production of H2S was mitigated in the LPS-induced MAC-T cells. Meanwhile, exogenous H2S decreased the intracellular ROS production and mRNA expression levels of the pro-inflammatory cytokines, TNF-α, IL-1β, IL-8, and IL-6. Furthermore, exogenous H2S inhibited the mRNA expression of TLR4 and activation of NF-κB signaling pathway. In summary, exogenous H2S exerts anti-inflammatory effects through attenuating oxidative stress and blocking the TLR4/NF-κB pathway in the LPS-induced bovine mammary epithelial cells. Our findings might clarify new prophylactic approaches for mastitis.
Keywords: Anti-inflammatory; Dairy mammary epithelial cells; Hydrogen sulfide; Lipopolysaccharide; NF-κB signaling pathways.
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