Puerarin inhibits Mycoplasma gallisepticum (MG-HS)-induced inflammation and apoptosis via suppressing the TLR6/MyD88/NF-κB signal pathway in chicken
Puerarin inhibits Mycoplasma gallisepticum (MG-HS)-induced inflammation and apoptosis via suppressing the TLR6/MyD88/NF-κB signal pathway in chicken
复制标题
葛根素通过抑制鸡体内Toll样受体6（TLR6）/髓样分化因子88（MyD88）/核因子κB（NF-κB）信号通路，减轻鸡毒支原体（MG-HS）诱导的炎症和细胞凋亡 。
DOI：
10.1016/j.intimp.2020.106993
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发表时间：
2020-11-01
影响因子：
5.6
通讯作者：
Peng, Xiuli
中科院分区：
文献类型：
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作者：
Niu, Lumeng;Luo, Ronglong;Peng, Xiuli
鸡毒支原体（Mycoplasma gallisepticum，MG）是引起鸡慢性呼吸道疾病（Chronic Respiratory Disease，CRD）的主要病原，主要引起宿主呼吸系统的炎症性损伤。以往的研究表明，葛根素（PUE）在炎症性疾病中起着关键的调节作用，而PUE对MG诱导的炎症的影响尚不清楚。本研究探讨了PUE对MG-HS感染的体内、外作用，表明其潜在的治疗和预防价值。实验结果表明，PUE明显抑制pMGA1.2的表达，通过减少细胞凋亡促进MG感染的细胞增殖和细胞周期进程。肺组织病理学检查显示MG感染组肺泡壁增厚、肺泡腔变窄、炎性细胞浸润严重。但PUE治疗可明显减轻MG所致的肺组织病理损伤。与MG感染组相比，PUE有效抑制MG诱导的炎症基因的表达，包括肿瘤坏死因子-α（TNF-α）、白细胞介素-1 β（IL-1 β）、细胞因子白细胞介素-6（IL-6）、toll样受体6（TLR 6）、髓样分化初级反应基因88（MyD 88）和核因子κ B（NF-κ B）。此外，PUE剂量依赖性地抑制MG诱导的NF-κ B p65进入细胞核。结论：PUE治疗可有效抑制MG诱导的炎症反应和细胞凋亡，通过抑制TLR 6/MyD 88/NF-κ B信号通路的激活，保护MG感染肺组织免受MG感染诱导的损伤。提示PUE可能是一种潜在的抗鸡MG感染的抗炎剂。
Mycoplasma gallisepticum (MG) is the primary etiological agent of chicken chronic respiratory disease (CRD), which mainly causes inflammatory damage of the host respiratory system. Previous studies suggest that puerarin (PUE) plays a pivotal regulatory role in inflammatory diseases, whereas the impacts of PUE on MG-induced inflammation remain unclear. This study investigated the effects of PUE on MG-HS infection in vitro and in vivo and indicated its potential therapeutic and preventive value. Experimental results showed that PUE significantly suppressed pMGA1.2 expression, promoted MG-infected cell proliferation and cell cycle process by reducing apoptosis. Histopathological examination of lung tissue showed severe histopathological lesions including thickened alveolar walls, narrowed alveolar cavity, and inflammatory cell infiltration in the MG-infected chicken group. However, PUE treatment significantly ameliorated MG-induced pathological damage in lung. Compared to the MG-infected group, PUE effectively inhibited the expression of MG-induced inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), cytokines interleukin-6 (IL-6), toll-like receptor 6 (TLR6), myeloid differentiation primary response gene 88 (MyD88) and nuclear factor kappa B (NF-kappa B). Moreover, PUE dose-dependently inhibited MG-induced NF-kappa B p65 to enter the cell nucleus. In conclusion, our findings indicate that PUE treatment can efficiently inhibit MG-induced inflammatory response and apoptosis, and protect the lung from MG infection-induced damage by inhibiting the TLR6/MyD88/NF-kappa B signaling pathway activation. The study suggests that PUE may be a potential anti-inflammatory agent defense against MG infection in chicken.