| 基于RAGE-TLR4串扰的高糖影响牛肺泡巨噬细胞促炎细胞因子释放的分子机制 |
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| 引用本文： | 谭天宇,才冬杰,苟丽萍,任志华,左之才.基于RAGE-TLR4串扰的高糖影响牛肺泡巨噬细胞促炎细胞因子释放的分子机制[J].畜牧兽医学报,2021,52(10):2944-2952. |
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| 作者姓名： | 谭天宇 才冬杰 苟丽萍 任志华 左之才 |
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| 作者单位： | 四川农业大学动物医学院, 动物疫病与人类健康四川省重点实验室, 成都 611130 |
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| 基金项目： | 四川省科技计划项目（2018NZ0002；2019YFQ0012）；国家重点研发计划项目（2018YFD0501800）；国家现代农业产业技术体系四川肉牛创新团队项目（SCCXTD-2020-13） |
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| 摘 要： | 本试验旨在研究高浓度葡萄糖对牛肺泡巨噬细胞（BAMs）促炎细胞因子IL-1β、IL-6及TNF-α释放的影响及其机制是否与RAGE-TLR4相关信号通路串扰有关。将BAMs随机分为正常糖组（NG）、高糖组（HG）、高糖+RAGE抑制剂组（H+F）、高糖+TLR4抑制剂组（H+T）及DMSO组，处理12 h后收集上清及下层细胞。采用qRT-PCR和Western blot检测细胞RAGE、TLR4、MyD88、NF-κB p65的mRNA及蛋白表达情况，ELISA检测上清TNF-α、IL-1β、IL-6浓度。结果表明，高糖极显著上调RAGE、TLR4、MyD88和NF-κB p65基因、蛋白表达水平以及上清液中IL-1β、IL-6、TNF-α浓度（P<0.01）；RAGE抑制剂与TLR4抑制剂均极显著抑制高糖引起的RAGE、TLR4、MyD88和NF-κB p65基因、蛋白表达水平上调以及IL-1β、IL-6、TNF-α释放（P<0.01），即RAGE与TLR4均在激活RAGE/TLR4/MyD88/NF-κB炎症信号通路中发挥调控作用。综上所述，高糖能够通过RAGE-TLR4串扰引起牛肺泡巨噬细胞释放促炎细胞因子IL-1β、IL-6及TNF-α，进一步阐明了高糖促进牛肺泡巨噬细胞炎症反应的分子机制。
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| 关 键 词： | 炎症信号通路 RAGE-TLR4串扰 牛肺泡巨噬细胞 高糖 |
| 收稿时间： | 2021-01-18 |
Molecular Mechanism of High Glucose Affecting Proinflammatory Cytokine Release from Bovine Alveolar Macrophages Based on RAGE-TLR4 Crosstalk |
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| TAN Tianyu,CAI Dongjie,GOU Liping,REN Zhihua,ZUO Zhicai.Molecular Mechanism of High Glucose Affecting Proinflammatory Cytokine Release from Bovine Alveolar Macrophages Based on RAGE-TLR4 Crosstalk[J].Acta Veterinaria et Zootechnica Sinica,2021,52(10):2944-2952. |
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| Authors: | TAN Tianyu CAI Dongjie GOU Liping REN Zhihua ZUO Zhicai |
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| Institution: | Sichuan Key Laboratory of Animal Diseases and Human Health, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China |
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| Abstract: | In this study, we aimed to investigate whether high glucose regulates proinflammatory cytokine IL-1β, IL-6 and TNF-α release from bovine alveolar macrophages (BAMs) through RAGE-TLR4 crosstalk. BAMs were randomly divided into normal glucose group (NG), high glucose group (HG), high glucose + RAGE inhibitor group (H + F), high glucose + TLR4 inhibitor group (H + T) and DMSO group, and the supernatant and lower cells were collected after 12 h of treatment. The mRNA and protein expression of RAGE, TLR4, MyD88 and NF-κB p65 were detected by qRT-PCR and Western blot, and the concentrations of TNF-α, IL-1β and IL-6 in the supernatant were detected by ELISA. The levels of mRNA and protein expression of RAGE, TLR4, MyD88 and NF-κB p65 and the concentrations of IL-1β, IL-6 and TNF-α in the supernatant of HG group were significantly higher than those of NG group, H+F group and H+T group (P<0.01); the levels of mRNA and protein of MyD88, NF-κB p65 and RAGE and the concentrations of three proinflammatory cytokines in the supernatant of H+F group and H+T group were significantly higher than those of NG group (P<0.05, P<0.01). Our results suggest that high glucose can cause the release of proinflammatory cytokines IL-1β, IL-6 and TNF-α from bovine alveolar macrophages via RAGE-TLR4 crosstalk, which further elucidated the molecular mechanism of high glucose promoted the inflammatory response in bovine alveolar macrophages. |
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| Keywords: | inflammatory signaling pathway RAGE-TLR4 crosstalk bovine alveolar macrophage high glucose |
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