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Expression of silent information regulator 1 in chronic rhinosinusitis and regulatory effects of inflammatory factors

机译:静音信息调节剂1在慢性鼻窦炎中的表达及炎症因子的调节作用

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摘要

We aimed to investigate the expression of silent information regulator 1 (Sirt1) in chronic rhinosinusitis (CRS) and the regulatory effects of inflammatory factors. The mucosal epithelial tissues of the nasal ethmoid sinus were collected from 30 patients with CRS from March 2017 to March 2019, and tissues from patients undergoing functional rhinoplasty were included as a control group. H&E staining and immunohistochemistry were performed to detect the histopathologic changes in the nasal mucosa and the expression of Sirt1. Epithelial cells in the control group were extracted from the ethmoid sinus mucosa and cultured in vitro. After the cells were treated with 0, 1, 10, and 100 ng/mL interleukin-5 (IL-5) and interferon-gamma (IFN-γ) for 24 h, qRT-PCR and western blotting were carried out to detect the mRNA and protein expressions of Sirt1. Nasal mucosal tissues of the control group were complete in structure, whereas large quantities of inflammatory cells infiltrated in nasal mucosa of the CRS group. Compared with the control group, the CRS group had significantly decreased protein and mRNA expression levels of Sirt1 (P<0.05), which significantly declined with increasing concentrations of IL-5 and IFN-γ (P<0.05). Thus, expression of Sirt1 in the nasal mucosa tissues of CRS patients is decreased, and inflammatory factors can reduce such expression in a dose-dependent manner. Sirt1 may participate in the inflammatory stress process of CRS.
机译:我们旨在探讨静音信息调节剂1(SIRT1)在慢性鼻窦炎(CRS)中的表达及炎症因素的调节作用。从2017年3月至2019年3月到2019年3月的30例CRS患者收集了鼻乙状体窦的粘膜上皮组织,并将接受功能鼻成形术的患者组织作为对照组。进行H&E染色和免疫组织化学以检测鼻粘膜的组织病理学变化和SIRT1的表达。从符号窦粘膜中提取对照组中的上皮细胞并在体外培养。在用0,1,10和100ng / ml白细胞介素-5(IL-5)处理细胞后,对24小时进行干扰素-γ(IFN-γ),进行QRT-PCR和Western印迹以检测SIRT1的mRNA和蛋白质表达。对照组的鼻粘膜组织结构在结构中完全,而在CRS组的鼻粘膜中渗入大量炎症细胞。与对照组相比,CRS组的蛋白质和mRNA表达水平显着降低(P <0.05),随着IL-5和IFN-γ的浓度增加而显着下降(P <0.05)。因此,降低了CRS患者的鼻粘膜组织中SIRT1的表达,并且炎症因素可以以剂量依赖性方式降低这些表达。 SIRT1可以参与CRS的炎症压力过程。

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