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羟基酪醇通过下调 NF-κB/NLRP3/IL-1β 信号通路减轻鸡传染性支气管炎病毒感染引起的肺损伤。

Hydroxytyrosol mitigates Mycoplasma gallisepticum-induced pulmonary injury through downregulation of the NF-κB/NLRP3/IL-1β signaling pathway in chicken.

机构信息

College of Animal Science, Guizhou University, Guiyang 550000, PR China.

Yunnan Academy of Forestry and Grassland, Kunming 650204, PR China.

出版信息

Poult Sci. 2023 May;102(5):102582. doi: 10.1016/j.psj.2023.102582. Epub 2023 Feb 17.

Abstract

In this study, the anti-inflammatory and antiapoptotic effects of hydroxytyrosol (HT) in Mycoplasma gallisepticum (MG)-infected chicken were investigated, and the underlying molecular mechanisms were explored. The results revealed severe ultrastructural pathological changes after MG infection in the lung tissue of chicken, including inflammatory cell infiltration, thickening of the lung chamber wall, visible cell swelling, mitochondrial cristae rupture, and ribosome shedding. MG possibly activated the nuclear factor κB (NF-κB)/nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)/interleukin (IL)-1β signaling pathway in the lung. However, HT treatment significantly ameliorated MG-induced pathological damage of the lung. HT reduced the magnitude of pulmonary injury after MG infection by reducing apoptosis and releasing the proinflammatory factors. Compared with the MG-infected group, the HT-treated group exhibited significant inhibition of the expression of NF-κB/NLRP3/IL-1β signaling-pathway-related genes; for example, the expressions of NF-κB, NLRP3, caspase-1, IL-1β, IL-2, IL-6, IL-18, and TNF-α significantly decreased (P < 0.01 or <0.05). In conclusion, HT effectively inhibited MG-induced inflammatory response and apoptosis and protected the lung by blocking the activation of NF-κB/NLRP3/IL-1β signaling pathway and reducing the damage caused by MG infection in chicken. This study revealed that HT may be a suitable and effective anti-inflammatory drug against MG infection in chicken.

摘要

在这项研究中,研究了羟基酪醇(HT)对感染鸡败血支原体(MG)的鸡的抗炎和抗凋亡作用,并探讨了其潜在的分子机制。结果显示,MG 感染后鸡肺组织出现严重的超微结构病理变化,包括炎症细胞浸润、肺腔壁增厚、可见细胞肿胀、线粒体嵴破裂和核糖体脱落。MG 可能通过激活核因子 κB(NF-κB)/核苷酸结合寡聚化结构域样受体蛋白 3(NLRP3)/白细胞介素(IL)-1β信号通路来感染鸡。然而,HT 处理可显著改善 MG 诱导的鸡肺损伤。HT 通过减少细胞凋亡和释放促炎因子来减轻 MG 感染引起的肺损伤。与 MG 感染组相比,HT 处理组 NF-κB/NLRP3/IL-1β 信号通路相关基因的表达明显受到抑制,例如 NF-κB、NLRP3、半胱天冬酶-1、IL-1β、IL-2、IL-6、IL-18 和 TNF-α 的表达明显降低(P<0.01 或<0.05)。总之,HT 通过阻断 NF-κB/NLRP3/IL-1β 信号通路的激活和减少 MG 感染对鸡的损伤,有效抑制了 MG 诱导的炎症反应和凋亡,保护了肺。本研究表明,HT 可能是一种有效的抗鸡败血支原体感染的抗炎药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ff1/10033309/8d9270912523/gr1.jpg

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