Chlorogenic acid, the primary active component in Chinese medicines like honeysuckle, exhibits anti-inflammatory and antiviral effects. It has been demonstrated that chlorogenic acid effectively prevents and treats Duck enteritis virus (DEV) infection. This study aims to further elucidate the mechanism by which chlorogenic acid prevents DEV infection. Duck embryo fibroblast (DEF) cells were pre-treated with chlorogenic acid before being infected with DEV. Cell samples were collected at different time points for transcriptomic sequencing, while qPCR was used to detect the proliferation of DEV. Additionally, 30-day-old ducks were treated with chlorogenic acid, and their lymphoid organs were harvested for histopathological sections to observe pathological damage. The proliferation of DEV in the lymphoid organs was also detected using qPCR Based on the transcriptomic sequencing results, NF-κB1 gene was silenced by RNAi technology to analyze the effect of NF-κB1 gene on DEV proliferation. Compared to the viral infection group, DEF cells in the chlorogenic acid intervention group exhibited significantly reduced DEV load (P < 0.05). Transcriptomic sequencing results suggested that chlorogenic acid inhibited DEV proliferation in DEF cells by regulating NF-κB signaling pathway. The results of RNAi silencing suggested that in the three treatment groups, compared with the DEV experimental group, there was no significant difference in the effect of pre-transfection after transfection on DEV proliferation, while both the pre-transfection after transfection and the simultaneous transfection group showed significant inhibition on DEV proliferation Furthermore, compared to the virus infection group, ducks in the chlorogenic acid intervention group showed significantly decreased DEV load in their lymphoid organs (P < 0.05), along with alleviated pathological damage such as nuclear pyretosis and nuclear fragmentation. Chlorogenic acid effectively inhibits DEV proliferation in DEF and duck lymphatic organs, mitigates viral-induced pathological damage, and provides a theoretical basis for screening targeted drugs against DEV.

中文翻译：

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绿原酸干预鸭瘟病毒感染鸭胚胎成纤维细胞的RNA-seq分析

绿原酸是金银花等中药的主要活性成分，具有抗炎、抗病毒作用。已证明绿原酸可有效预防和治疗鸭肠炎病毒（DEV）感染。本研究旨在进一步阐明绿原酸预防DEV感染的机制。鸭胚胎成纤维细胞 (DEF) 在感染 DEV 之前用绿原酸进行预处理。不同时间点采集细胞样本进行转录组测序，同时采用qPCR检测DEV增殖情况。另外，对30日龄鸭进行绿原酸处理，收获其淋巴器官进行组织病理学切片，观察病理损伤。采用qPCR检测淋巴器官中DEV的增殖情况。根据转录组测序结果，采用RNAi技术沉默NF-κB1基因，分析NF-κB1基因对DEV增殖的影响。与病毒感染组相比，绿原酸干预组DEF细胞DEV载量显着降低（P < 0.05）。转录组测序结果表明，绿原酸通过调节NF-κB信号通路抑制DEF细胞中DEV增殖。RNAi沉默结果提示，三个处理组中，与DEV实验组相比，转染后预转染对DEV增殖的影响无显着差异，而转染后预转染和同时转染均无显着差异。此外，与病毒感染组相比，绿原酸干预组鸭淋巴器官DEV负荷显着降低（P < 0.05），核热焦、核碎裂等病理损伤减轻。绿原酸有效抑制DEF和鸭淋巴器官中DEV增殖，减轻病毒引起的病理损伤，为筛选抗DEV靶向药物提供理论依据。