Liu Kangjun, Qiu Shangfei, Fang Li, Cui Luying, Dong Junsheng, Guo Long, Meng Xia, Li Jianji, Wang Heng
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
International Research Laboratory of Prevention and Control of Important Animal Infectious Diseases and Zoonotic Diseases of Jiangsu Higher Education Institutions, Yangzhou 225009, China.
Vet Sci. 2024 Nov 29;11(12):607. doi: 10.3390/vetsci11120607.
() 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 are unclear. In the present study, primary BMECs were infected with 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 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 -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 .
()是与奶牛临床乳腺炎相关的一种重要病原体。在临床乳腺炎期间,抗炎药物对于减轻疼痛和炎症是必要的。在众多药物中,美洛昔康(MEL)因其对环氧合酶-2(COX-2)酶具有出色的抑制作用而被广泛用于临床乳腺炎。然而,MEL对由(此处原文缺失病原体名称)诱导的炎症反应和氧化应激的有效性尚不清楚。在本研究中,在存在或不存在血浆维持浓度的MEL(0.5和5μM)的情况下,用(此处原文缺失病原体名称)感染原代乳腺上皮细胞(BMECs)。在用(此处原文缺失病原体名称)和MEL联合处理1或3小时后,收集BMECs以评估相关指标。结果表明,血浆维持浓度的MEL对未感染的BMECs的活力没有影响,对BMECs中的细菌载量也没有影响。在这些浓度下,MEL能够抑制COX-2、白细胞介素(IL)-1β、肿瘤坏死因子α(TNF-α)和IL-6的mRNA表达,同时提高感染(此处原文缺失病原体名称)的BMECs中IL-8的mRNA水平。MEL通过增加超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性以及总抗氧化能力(T-AOC)水平,对减轻氧化应激具有明显作用。MEL减轻炎症反应和氧化应激的机制部分归因于对核转录因子-κB(NF-κB)信号通路的抑制以及核因子红细胞2相关因子(Nrf2)信号通路激活的改善。总之,结果表明血浆维持浓度的MEL可保护BMECs免受由(此处原文缺失病原体名称)诱导的炎症和氧化损伤。