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Naringin's Alleviation of the Inflammatory Response Caused by Actinobacillus pleuropneumoniae by Downregulating the NF-κB/NLRP3 Signalling Pathway

文献类型： 外文期刊

作者： Huang, Qilin 1 ; Li, Wei 4 ; Jing, Xiaohan 1 ; Liu, Chen 1 ; Ahmad, Saad 1 ; Huang, Lina 5 ; Zhao, Guanyu 1 ; Li, Zhaorong 1 ; Qiu, Zhengying 1 ; Xin, Ruihua 1 ;

作者机构： 1.Chinese Acad Agr Sci CAAS, Lanzhou Inst Husb & Pharmaceut Sci, Lanzhou 730050, Peoples R China

2.Engn & Technol Res Ctr Tradit Chinese Vet Med Gans, Lanzhou 730050, Peoples R China

3.Minist Agr & Rural Affairs China, Key Lab Vet Pharmaceut Dev, Lanzhou 730050, Peoples R China

4.Lanzhou Ctr Anim Dis Control & Prevent, Lanzhou 730050, Peoples R China

5.Lanzhou Univ, Sch Pharm, State Key Lab Appl Organ Chem, Lanzhou 730013, Peoples R China

关键词： Actinobacillus pleuropneumoniae (APP); inflammatory injury; NLRP3 inflammasome; protein interactions; naringin (NAR); anti-inflammatory mechanism

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：5.6； 五年影响因子：6.2 ）

ISSN： 1661-6596

年卷期： 2024 年 25 卷 2 期

页码：

收录情况： SCI

摘要： Actinobacillus pleuropneumoniae (APP) is responsible for causing Porcine pleuropneumonia (PCP) in pigs. However, using vaccines and antibiotics to prevent and control this disease has become more difficult due to increased bacterial resistance and weak cross-immunity between different APP types. Naringin (NAR), a dihydroflavonoid found in citrus fruit peels, has been recognized as having significant therapeutic effects on inflammatory diseases of the respiratory system. In this study, we investigated the effects of NAR on the inflammatory response caused by APP through both in vivo and in vitro models. The results showed that NAR reduced the number of neutrophils (NEs) in the bronchoalveolar lavage fluid (BALF), and decreased lung injury and the expression of proteins related to the NLRP3 inflammasome after exposure to APP. In addition, NAR inhibited the nuclear translocation of nuclear factor kappa-B (NF-kappa B) P65 in porcine alveolar macrophage (PAMs), reduced protein expression of NLRP3 and Caspase-1, and reduced the secretion of pro-inflammatory cytokines induced by APP. Furthermore, NAR prevented the assembly of the NLRP3 inflammasome complex by reducing protein interaction between NLRP3, Caspase-1, and ASC. NAR also inhibited the potassium (K+) efflux induced by APP. Overall, these findings suggest that NAR can effectively reduce the lung inflammation caused by APP by inhibiting the over-activated NF-kappa B/NLRP3 signalling pathway, providing a basis for further exploration of NAR as a potential natural product for preventing and treating APP.

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