H 2 S mediates apoptosis in response to inflammation through PI3K/Akt/NFκB signaling pathway

Hydrogen sulfide (H S) is involved in regulating cell apoptosis and proliferation. However, The effects and mechanism of H S on the apoptosis of mammary epithelial cells that suffer from an inflammatory response remain unknown. An inflammatory cell model was used to explore whether exogenous H S regulates lipopolysaccharides (LPS)-induced cell proliferation and apoptosis. We found that H S affected cell viability, the inflammatory response and apoptosis in LPS-treated cells in a concentration-dependent manner. Moreover, exogenous H S rescued LPS-induced cystathionine γ-lyase (CSE) inhibition and cystathionine β-synthase (CBS) synthesis. Interestingly, in cells undergoing inflammation-induced apoptosis, H S activated the PI3K/Akt and NFκB signal pathways both tested concentrations. Akt appeared to be a key crosstalk molecule that played a "bridge" role. H S regulates LPS-induced inflammation and apoptosis by activating the PI3K/Akt/NFκB signaling pathway. Hence, NaHS may be clinically useful for preventing or treating mastitis.