The protective effect of caffeic acid against inflammation injury of primary bovine mammary epithelial cells induced by lipopolysaccharide

Abstract

Caffeic acid possesses multiple biological effects, such as antibacterial, antioxidant, antiinflammatory, and anticancer growth; however, what effects it has on bovine mastitis have not been investigated. The aim of this study was to verify the antiinflammatory properties of caffeic acid on the inflammatory response of primary bovine mammary epithelial cells (bMEC) induced by lipopolysaccharide (LPS), and to clarify the possible underlying mechanism. Bovine mammary epithelial cells were treated with various concentrations (10, 50, 100, and 200 μg/mL) of LPS for 3, 6, 12, and 18 h; the results showed that LPS significantly inhibited cell viability in a time- and dose-dependent manner. When cells were treated with LPS (50 μg/mL) for 12h, the cell membrane permeability significantly increased, which promoted cell apoptosis. Various concentrations (10, 25, and 50 μg/mL) of caffeic acid could weaken the inflammation injury of bMEC induced by LPS without cytotoxicity. Proinflammatory cytokines (IL-8, IL-1β, IL-6, and tumor necrosis factor α) from bMEC were decreased. Nuclear transcription factor κB activity was weakened via blocking κB inhibitor α degradation and p65 phosphorylation. All these showed that the protective effect of caffeic acid on LPS-induced inflammation injury in bMEC was at least partly achieved by the decreased production of proinflammatory cytokines mediated by the effect of reducing the κB inhibitor α degradation and p65 phosphorylation in the nuclear transcription factor κB pathway. The use of caffeic acid would be beneficial in dairy cows during Escherichia coli mastitis as a safe and natural antiinflammatory drug.

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

“…The interaction between LPS and TLR4 results in the activation of intracellular signaling through myeloid differentiation factor 88 (MyD88) and TIR-domain-containing adapter-inducing interferon-β (TRIF) pathways, leading to the activation of major mitogen-activated protein kinases (MAPKs) and translocation of nuclear transcription factor-κB (NF-κB) (Sheldon and Roberts, 2010;Kawai and Akira, 2011;Huang et al, 2016). NF-κB regulates the expression of cytokines, including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α), which are essential mediators of the inflammation response (Wang et al, 2012;Liu et al, 2014;Huang et al, 2016).…”

Bovine recombinant lipopolysaccharide binding protein (BRLBP) regulated apoptosis and inflammation response in lipopolysaccharide-challenged bovine mammary epithelial cells (BMEC)

“…2A). This was consistent with previous reports (Wellnitz and Kerr, 2004;Liu et al, 2014). In this study, LPS-induced inflammation injury of BMEC was assessed ( Fig.…”

“…Apoptosis is involved in multiple organ dysfunction during septic shock (Hotchkiss et al, 1999). LPS has been shown to induce apoptosis in multiple cell types, such as macrophages and BMECs (Xaus et al, 2000;Liu et al, 2014). Current data showed that LPS stimulation demonstrated time and dosedependent effects on the viability of BMECs ( Fig.…”

Anti-Inflammatory Effects of Chamaecyparis Obtusa Essential Oil on Peripheral Blood Mononuclear Cells

“…Cells were treated with LPS at concentrations of 0, 1, and 25 µg/ml for various time points depending on each experimental settings. LPS concentrations were chosen based on previous studies by others using mammary epithelial cells [18,20]. In the experiments for testing the effects of pharmacological inhibitors, cells were pretreated with the inhibitors (PD98059, LY294002, and SB203580) at 20 and 40 µM for 1 h, followed by stimulation with LPS at 0, 1, and 25 µg/ml for 12 h.…”

“…These LPS concentrations were also chosen by others when treating mammary epithelial cells, owing to the capability of cell challenging without significant cell death [18,20].…”