Yi Dandan, Wang Menghui, Liu Xia, Qin Lanqian, Liu Yu, Zhao Linyi, Peng Ying, Liang Zhengmin, He Jiakang
College of Animal Science and Technology, Guangxi University, Nanning 530004, China.
Guangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, Nanning 530004, China.
Antioxidants (Basel). 2024 Oct 18;13(10):1265. doi: 10.3390/antiox13101265.
() infection disrupts the homeostasis of the intestinal microbiota, causing an intestinal inflammatory response and posing a great threat to human and animal health. The unreasonable use of antibiotics has led to an increase in the prevalence of drug-resistant , increasing the difficulty of controlling . Therefore, new drug strategies and research are urgently needed to control . Rosmarinic acid (RA) is a natural phenolic acid with various pharmacological activities, including antioxidant, anti-inflammatory and antibacterial properties. However, the protective effects and mechanism of RA on intestinal inflammation and the gut microbial disorders caused by have not been fully elucidated. In this study, RAW264.7 cells, MCECs and BALB/c mice were challenged with to assess the protective effects and mechanisms of RA. The results showed that RA enhanced the phagocytic ability of RAW264.7 cells, reduced the invasion and adhesion ability of in MCECs, and inhibited -induced inflammation in cells. Moreover, RA inhibited the activation of the NF-κB signaling pathway by upregulating TLR9 expression. Importantly, we found that RA provided protection against and increased the diversity and abundance of the intestinal microbiota in mice. Compared with infection control, RA significantly increased the abundance of and and decreased the abundance of , and . However, RA failed to alleviate -induced inflammation and lost its regulatory effects on the TLR9/NF-κB signaling pathway after destroying the gut microbiota with broad-spectrum antibiotics. These results indicated that RA attenuated -induced inflammation by regulating the TLR9/NF-κB signaling pathway and maintaining the homeostasis of the gut microbiota. Our study provides a new strategy for preventing -induced intestinal inflammation.
()感染会破坏肠道微生物群的稳态,引发肠道炎症反应,对人类和动物健康构成巨大威胁。抗生素的不合理使用导致耐药性患病率增加,加大了控制的难度。因此,迫切需要新的药物策略和研究来控制()。迷迭香酸(RA)是一种具有多种药理活性的天然酚酸,包括抗氧化、抗炎和抗菌特性。然而,RA对()引起的肠道炎症和肠道微生物紊乱的保护作用及机制尚未完全阐明。在本研究中,用()刺激RAW264.7细胞、MCECs和BALB/c小鼠,以评估RA的保护作用和机制。结果表明,RA增强了RAW264.7细胞的吞噬能力,降低了()在MCECs中的侵袭和黏附能力,并抑制了()诱导的细胞炎症。此外,RA通过上调TLR9表达抑制NF-κB信号通路的激活。重要的是,我们发现RA对()具有保护作用,并增加了小鼠肠道微生物群的多样性和丰度。与感染对照组相比,RA显著增加了()和()的丰度,降低了()、()和()的丰度。然而,在用广谱抗生素破坏肠道微生物群后,RA未能减轻()诱导的炎症,且失去了对TLR9/NF-κB信号通路的调节作用。这些结果表明,RA通过调节TLR9/NF-κB信号通路和维持肠道微生物群的稳态来减轻()诱导的炎症。我们的研究为预防()诱导的肠道炎症提供了一种新策略。