Wan Zhiling, Liu Ting, Cheng Anchun, Li Hui, Lin Rutao, Zhu Erpeng, Huang Yao, Liu Shunxing, Tang Yu, Shan Chunlan, Cheng Zhentao
College of Animal Science, Guizhou University, Guiyang, 550025, China.
College of Animal Science, Guizhou University, Guiyang, 550025, China; Institute of Veterinary Immunology and Green Drugs, Veterinary Department in College of Aminal Science, State Key Laboratory of Green Pesticide, Guizhou University, Guiyang 550025, China.
Poult Sci. 2025 Jun 30;104(10):105485. doi: 10.1016/j.psj.2025.105485.
Mycoplasma gallisepticum (MG) is a pathogen commonly found in poultry that can cause avian-associated respiratory diseases. Arbutin (AR) possesses various pharmacological activities, including anti-tumor, anti-inflammatory, apoptotic regulation, and anti-oxidative stress effects, however, its impact and mechanisms against inflammatory damage caused by MG infection remain unclear. The results demonstrated that after AR intervention, the MG-induced symptoms such as pulmonary wall thickening, lung tissue congestion and hemorrhage, inflammatory cell infiltration, and HD11 cell swelling were significantly ameliorated. Antioxidant activity increased, and the expression of KUL01 protein and transcription levels of chemokines in macrophages decreased significantly. MG infection activated the nuclear factor-κB (NF-κB)/nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) signaling pathway in lung tissue, and AR intervention effectively regulated the expression of apoptosis genes, significantly inhibiting the transcription levels of NF-κB, NLRP3, Caspase-1, IL-1β, IL-18, and TNF-α genes within the pathway. The effect of AR on the NLRP3 target gene in MG infection was further confirmed through HD11 cell experiments. These results indicated that AR could reduce the damage caused by MG infection and effectively inhibit apoptosis, oxidative stress, and macrophage response induced by the infection, primarily through the regulation of the NF-κB/NLRP3 signaling pathway to protect the lung.
鸡毒支原体(MG)是一种常见于家禽中的病原体,可引发禽类相关呼吸道疾病。熊果苷(AR)具有多种药理活性,包括抗肿瘤、抗炎、凋亡调控和抗氧化应激作用,然而,其对MG感染所致炎症损伤的影响及机制仍不清楚。结果表明,AR干预后,MG诱导的诸如肺壁增厚、肺组织充血和出血、炎性细胞浸润以及HD11细胞肿胀等症状明显改善。抗氧化活性增强,巨噬细胞中KUL01蛋白表达及趋化因子转录水平显著降低。MG感染激活了肺组织中的核因子κB(NF-κB)/核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)信号通路,AR干预有效调节凋亡基因的表达,显著抑制该通路中NF-κB、NLRP3、半胱天冬酶-1、白细胞介素-1β、白细胞介素-18和肿瘤坏死因子-α基因的转录水平。通过HD11细胞实验进一步证实了AR对MG感染中NLRP3靶基因的作用。这些结果表明,AR可减轻MG感染造成的损伤,并有效抑制感染诱导的凋亡、氧化应激和巨噬细胞反应,主要是通过调节NF-κB/NLRP3信号通路来保护肺部。