The Effect of Meloxicam on Inflammatory Response and Oxidative Stress Induced by Klebsiella pneumoniae in Bovine Mammary Epithelial Cells

<i>Klebsiella pneumoniae</i> (<i>K. pneumoniae</i>) is a significant pathogen associated with clinical mastitis in cattle. Anti-inflammatory drugs are necessary to alleviate pain and inflammation during clinical mastitis. Among many drugs, meloxicam (MEL) has been widely used in clinical mastitis because of its excellent inhibitory effect on the cyclooxygenase-2 (COX-2) enzyme. However, the effectiveness of MEL on the inflammatory response and oxidative stress induced by <i>K. pneumoniae</i> are unclear. In the present study, primary BMECs were infected with <i>K. pneumoniae</i> in the presence or absence of plasma maintenance concentration of MEL (0.5 and 5 μM). Following 1 or 3 h of combined treatment with <i>K. pneumoniae</i> and MEL, BMECs were gathered to assess the related indicators. The results showed that MEL at plasma maintenance concentrations exerted no influence on the viability of uninfected BMECs and also had no impact on bacterial load in BMECs. At these concentrations, MEL was able to inhibit the mRNA expression of COX-2, Interleukin (IL)-1β, Tumor necrosis factor α (TNF-α), and IL-6 while simultaneously elevating the mRNA levels of IL-8 in <i>K. pneumoniae</i>-infected BMECs. MEL had clear effects on relieving oxidative stress by increasing the activity of superoxide dismutase (SOD) and catalase (CAT) and the level of total antioxidant capacity (T-AOC). The mechanisms by which MEL mitigated the inflammatory response and oxidative stress were partially attributed to inhibition of the nuclear transcription factor-kappa B (NF-κB) signaling pathway and improvement of the activation of the nuclear factor erythroid 2-related factors (Nrf2) signaling pathway. To conclude, the results manifested that MEL at plasma maintenance concentrations protected BMECs from inflammatory and oxidative damage induced by <i>K. pneumoniae</i>.