Glutamine pretreatment protects bovine mammary epithelial cells from inflammation and oxidative stress induced by γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP)

Glutamine (GLN) has many types of biological activity in rats, including anti-inflammatory, antioxidative stress, and anti-apoptosis effects. However, little is known about the effects GLN on bovine mammary epithelial cells (BMEC). γ-d-Glutamyl-meso-diaminopimelic acid (iE-DAP) a cell wall peptidoglycan component gram-negative bacteria that can be recognized by intracellular receptor nucleotide-binding oligomerization domain-containing protein 1 (NOD1) cause mastitis. The goal present study was to investigate whether protects BMEC from iE-DAP–induced inflammation, oxidative apoptosis. We cultured GLN-free medium for 24 h then separated them into 4 groups: treated with 1× PBS 26 or 32 (control); stimulated 10 μg/mL iE-DAP 2 8 (2- 8-h iE-DAP); pretreated mM followed treatment (8 GLN); (DG). In 2-h group, when levels inflammation peaked, increased both mRNA expression NOD1, inhibitor nuclear factor-κB (NFKBIA, IκB), subunit p65 (RELA, NF-κB p65), as well IL6 IL8 IL-6 tumor necrosis factor-α culture supernatants. contrast, pretreatment inhibited inflammatory-related factors suppressing NOD1/NF-κB pathway. decreased extracellular regulated kinase (Erk, ERK) factor erythroid 2–associated factor2 (NFE2L2, Nrf2), superoxide dismutase (SOD1), catalase (CAT), coenzyme II oxidoreductase (NQO1), heme oxygenase (HMOX1, HO1). addition, malondialdehyde stress peaked. Interestingly, induced stress–related reactive oxygen species promoting ERK/Nrf2 Moreover, reduced apoptosis caused BMEC. This first report showing against iE-DAP-induced via pathways