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虎杖苷通过抑制 TLR6/MyD88/NF-κB 通路减轻鸡毒支原体(HS 株)诱导的炎症损伤。

Polydatin attenuates Mycoplasma gallisepticum (HS strain)-induced inflammation injury via inhibiting the TLR6/ MyD88/NF-κB pathway.

机构信息

Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education, College of Animal Science and Technology and College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.

Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education, College of Animal Science and Technology and College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.

出版信息

Microb Pathog. 2020 Dec;149:104552. doi: 10.1016/j.micpath.2020.104552. Epub 2020 Sep 30.

DOI:10.1016/j.micpath.2020.104552
PMID:33010363
Abstract

Mycoplasma gallisepticum (MG) infection is the main cause of chronic respiratory disease (CRD) characterized by severe respiratory inflammation in chickens. Polydatin (PD) is a resveratrol glycoside isolated from Polygonum cuspidatum, which has prominent anti-inflammatory effect. The purpose of this study was to investigate the therapeutic effect of PD against MG-induced inflammation in chicken and its underlying mechanism. Histopathological analysis showed that PD treatment (15, 30, and 45 mg/kg) apparently alleviated MG-induced pathological changes of chicken embryonic lung. In chicken embryo fibroblast (DF-1) cells, PD treatment (15, 30, and 60 μg/mL) could effectively suppress MG propagation, promote MG-infected cell proliferation and cell cycle progress, and inhibit MG-induced cell apoptosis. ELISA and qPCR assays showed that PD treatment significantly suppressed the expression of interleukin-6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α) induced by MG both in vivo and in vitro. Besides, molecular studies indicated that the MG-induced levels of toll-like receptor-6 TLR6, myeloid differentiation-88 (MyD88) and nuclear factor κB (NF-κB) were significantly decreased by PD treatment. Moreover, immunofluorescence analysis showed that PD treatment restrained the MG-induced NF-κB-p65 nuclear translocation. Taken together, these results indicate the protective effects of PD against MG-induced inflammation injury in chicken were mainly by inhibiting the TLR6/MyD88/NF-κB pathway.

摘要

鸡败血支原体(MG)感染是慢性呼吸道病(CRD)的主要病因,其特征是鸡严重的呼吸道炎症。虎杖苷(PD)是从虎杖中分离得到的白藜芦醇糖苷,具有显著的抗炎作用。本研究旨在探讨 PD 对 MG 诱导的鸡炎症的治疗作用及其机制。组织病理学分析表明,PD 治疗(15、30 和 45mg/kg)明显减轻了 MG 诱导的鸡胚肺的病理变化。在鸡胚成纤维细胞(DF-1)中,PD 治疗(15、30 和 60μg/mL)可有效抑制 MG 的增殖,促进 MG 感染细胞的增殖和细胞周期进程,并抑制 MG 诱导的细胞凋亡。ELISA 和 qPCR 检测表明,PD 治疗可显著抑制 MG 在体内和体外诱导的白细胞介素-6(IL-6)、IL-1β和肿瘤坏死因子-α(TNF-α)的表达。此外,分子研究表明,PD 治疗可显著降低 MG 诱导的 toll 样受体 6(TLR6)、髓样分化因子 88(MyD88)和核因子 κB(NF-κB)水平。此外,免疫荧光分析表明,PD 治疗抑制了 MG 诱导的 NF-κB-p65 核转位。综上所述,这些结果表明 PD 对 MG 诱导的鸡炎症损伤具有保护作用,主要是通过抑制 TLR6/MyD88/NF-κB 通路。

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