Abstract
Ammonia is one of the major toxic components of metabolites in blood and tissues of high-producing dairy cows and could affect the health of bovine mammary glands. Bovine mammary epithelial cells are sensitive to oxidative stress induced by intensive cell metabolism. In our previous study, we found that ammonia could induce oxidative stress, apoptosis and inflammatory responses in bovine mammary epithelial cells. In the present study, the cytoprotective effects of astragaloside IV against ammonia in vitro were explored. The results demonstrated that pretreatment of MAC-T cells with astragaloside IV could potently suppress the increase in the level of intracellular reactive oxygen species (ROS) and the rate of cell apoptosis, inhibit the ammonia-induced inflammatory responses, and rescue the decrease of cell viability. Astragaloside IV prevented ammonia-induced endoplasmic reticulum stress. Astragaloside IV also significantly suppressed the levels of BAX, caspase 3 and p53 phosphorylation in ammonia-induced MAC-T cells. Nuclear factor erythroid 2-related factor 2(Nrf2) was essential for cytoprotective effects of astragaloside IV in MAC-T cells, as knockdown of Nrf2 dramatically abolished the prosurvival effects of astragaloside IV on treated cells. Furthermore, the PI3K/AKT and ERK/MAPK pathways were responsible for the induction of Nrf2 by astragaloside IV. In conclusion, astragaloside IV played a beneficial role against ammonia-induced damage of MAC-T cells. This provides a cue for future study to use astragaloside IV as a protective and curative agent against ammonia exposure of mammary glands in dairy cows.
Highlights
Ammonia, produced mainly from the deamination of amino acids and glutamine, is one of the major toxic components in blood and tissues that may affect bovine health [1]
We found that ammonia could induce oxidative stress and apoptosis in bovine mammary epithelial cells [3]
The results showed that astragaloside IV at the concentrations of 5, 10, and 20 μM suppressed the production of IL8 and IL-6 in ammonia-treated MAC-T cells (Figure 4)
Summary
Ammonia, produced mainly from the deamination of amino acids and glutamine, is one of the major toxic components in blood and tissues that may affect bovine health [1]. We found that ammonia could induce oxidative stress and apoptosis in bovine mammary epithelial cells [3]. Reasgualitnsst ammonia-induced oxidative stress and apoptosis of bovine mammary epithelial cells. E2f.feRctesouf lAtsstragaloside IV on Ammonia-Induced Bovine Mammary Epithelial Cell Death. The effects of astragaloside IV on p53 signaling pathways induced by ammonia in MAC-T cells wereTvheeriefifefedctvsiaofWasetsrtaegrnalobsloidtteinIVg. oAnsps5h3oswignnainlinFgigpuarteh3w, aaymsminodnuicaesdigbnyifiacmamntolyniuapin-reMgAulCat-eTdcethlles lweveerelsvoefrpif-ipe5d3v, ciaonWsiesstetenrtnwbitlhototiunrgp. The results showed that astragaloside IV at the concentrations of 5, 10, and 20 μM suppressed the production of IL8 and IL-6 in ammonia-treated MAC-T cells (Figure 4). Fituiornth, earnmionrhei,bkintoorcykdefofwecnt of Nasrtfr2agabaloolsisidhedIVtheonprtohteecmtivReNeAffeecxtporfeasstiorangaolfoCsiHdeOIPV wagaasinsottasnhoawmnmoinnitah-einNdurfc2edsiRdeNcAre-atsreaninsfceecltledviacbelilsity(F(iFgiugruere6B6C).)F. urthermore, knockdown of Nrf abolished the protective effect of astragaloside IV against an ammonia-induced decrease in cell viability (Figure 6C). PD98059 and LY294002 abrogated the ROS scavenging effects of astragaloside IV (Figure 8B)
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