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熊果苷通过JAK2/STAT3信号通路减轻鸡毒支原体诱导的肺纤维化损伤。

Arbutin alleviates Mycoplasma gallinarum-induced damage caused by pulmonary fibrosis via the JAK2/STAT3 pathway.

作者信息

Liu Ting, Cheng Zhentao, Song Derong, Zhu Erpeng, Li Hui, Lin Rutao, Wan Zhiling, Liu Shunxing, Gong Zeguang, Shan Chunlan

机构信息

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

Bijie Institute of Animal Husbandry and Veterinary Sciences, Bijie, 551700, PR China.

出版信息

Poult Sci. 2024 Dec;103(12):104434. doi: 10.1016/j.psj.2024.104434. Epub 2024 Oct 19.

DOI:10.1016/j.psj.2024.104434
PMID:39467406
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11550161/
Abstract

Mycoplasma gallinarum (MG) can cause infectious respiratory diseases in poultry that are chronic. Arbutin (AR) possesses anti-inflammatory, bacteriostatic, antitussive, and expectorant pharmacological effects, but whether it exerts regulatory effects on MG-induced pneumonia and fibrosis remains unclear. The study results unveiled that pulmonary connective tissue hyperplasia, pulmonary capillary congestion, and inflammatory cell infiltration, as well as serum levels of cytokines (i.e., TNF-α, IL-1β, IL-6, and IL-10), were elevated after MG infection. Collagen fibers were significantly deposited in the lung tissue from MG-infected chicks. Furthermore, the expression levels of key factors in the JAK2/STAT3 and TGF-β/Smad pathways markedly increased. AR intervention significantly alleviated MG-induced pneumonic injury, and reduced collagen deposition and the expression of fibrosis markers in the lung tissue. AR reduced the degree of pulmonary fibrosis by regulating key factors of the JAK2/STAT3 signaling pathway in the MG-infected HD11 cells. Thus, AR effectively reduced the expression of inflammatory factors by regulating the JAK2/STAT3 signaling pathway, thereby improving lung inflammation and fibrosis.

摘要

鸡毒支原体(MG)可引发家禽慢性传染性呼吸道疾病。熊果苷(AR)具有抗炎、抑菌、镇咳和祛痰的药理作用,但它是否对MG诱导的肺炎和纤维化发挥调节作用仍不清楚。研究结果表明,MG感染后,肺结缔组织增生、肺毛细血管充血、炎性细胞浸润以及细胞因子(即肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6和白细胞介素-10)的血清水平均升高。MG感染雏鸡的肺组织中胶原纤维显著沉积。此外,JAK2/STAT3和TGF-β/Smad信号通路中关键因子的表达水平明显增加。AR干预显著减轻了MG诱导的肺部损伤,并减少了肺组织中的胶原沉积和纤维化标志物的表达。AR通过调节MG感染的HD11细胞中JAK2/STAT3信号通路的关键因子,降低了肺纤维化程度。因此,AR通过调节JAK2/STAT3信号通路有效降低了炎性因子的表达,从而改善了肺部炎症和纤维化。

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Biomed Pharmacother. 2024 Feb;171:116138. doi: 10.1016/j.biopha.2024.116138. Epub 2024 Jan 18.
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Targeting the JAK2/STAT3 signaling pathway for chronic pain.针对 JAK2/STAT3 信号通路治疗慢性疼痛。
Aging Dis. 2024 Feb 1;15(1):186-200. doi: 10.14336/AD.2023.0515.
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Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model.
小分子介导的 OGG1 抑制可减轻小鼠肺纤维化模型中的肺部炎症和肺纤维化。
Nat Commun. 2023 Feb 6;14(1):643. doi: 10.1038/s41467-023-36314-5.
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Silencing FHL2 inhibits bleomycin-induced pulmonary fibrosis through the TGF-β1/Smad signaling pathway.沉默 FHL2 通过 TGF-β1/Smad 信号通路抑制博来霉素诱导的肺纤维化。
Exp Cell Res. 2023 Feb 15;423(2):113470. doi: 10.1016/j.yexcr.2023.113470. Epub 2023 Jan 11.
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