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首页> 外文期刊>Food Science & Nutrition >NF‐κB‐mediated inflammatory damage is differentially affected in SH‐SY5Y and C6 cells treated with 27‐hydroxycholesterol
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NF‐κB‐mediated inflammatory damage is differentially affected in SH‐SY5Y and C6 cells treated with 27‐hydroxycholesterol

机译：NF-κB介导的炎性损伤在用27-羟基胆固醇处理的SH-SY5Y和C6细胞中受到不同的影响

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Previous studies have demonstrated that 27‐hydroxycholesterol (27‐OHC), a cholesterol metabolite, was involved in the inflammatory process of Alzheimer's disease (AD). The present study aimed to investigate the 27‐OHC‐induced inflammatory damage to neurons and astrocytes and the underlying mechanism(s) accounting for this damage. Human neuroblastoma cells (SH‐SY5Y cells) and rat glioma cells (C6 cells) were treated with vehicle or 27‐OHC (5, 10, or 20?μM) for 24?hr. The levels of secreted interleukin‐1β (IL‐1β), interleukin‐10 (IL‐10), tumor necrosis factor alpha (TNF‐α), and inducible nitric oxide synthase (iNOS) were determined by using an enzyme‐linked immunosorbent assay (ELISA). Immunofluorescence staining was used to determine the cellular expression of toll‐like receptor 4 (TLR4) and transforming growth factor‐β (TGF‐β). The mRNA and protein expression levels of nuclear factor‐κB p65 (NF‐κB p65), nuclear factor‐κB p50 (NF‐κB p50) and cyclooxygenase‐2 (COX‐2) in both SH‐SY5Y and C6 cells were also detected by real‐time PCR and Western blot, respectively. The results of this study showed that 27‐OHC treatment increased secretion of TNF‐α and iNOS and decreased secretion of IL‐10, upregulated expression of TGF‐β, NF‐κB p65 and p50, and downregulated expression of COX‐2 in SH‐SY5Y cells. In C6 cells, treatment with 27‐OHC resulted in decreased secretion of IL‐1β, IL‐10, TNF‐α, and iNOS, and increased expression of TLR4 and TGF‐β. These results suggest that 27‐OHC may cause inflammatory damage to neurons by activating the TGF‐β/NF‐κB signaling pathway and to astrocytes by activating the TLR4/TGF‐β signaling, which results in the subsequent release of inflammatory cytokines.
机译：先前的研究表明，胆固醇代谢产物27-羟基胆固醇（27-OHC）参与了阿尔茨海默氏病（AD）的炎症过程。本研究旨在调查27-OHC诱导的神经元和星形胶质细胞炎症性损害，以及造成这种损害的潜在机制。将人类神经母细胞瘤细胞（SH-SY5Y细胞）和大鼠神经胶质瘤细胞（C6细胞）分别用赋形剂或27-OHC（5、10或20？M）处理24小时。使用酶联免疫吸附测定法测定分泌的白介素-1β（IL-1β），白介素-10（IL-10），肿瘤坏死因子α（TNF-α）和诱导型一氧化氮合酶（iNOS）的水平（ELISA）。免疫荧光染色用于确定Toll样受体4（TLR4）和转化生长因子β（TGF-β）的细胞表达。还检测到SH‐SY5Y和C6细胞中核因子κBp65（NF‐κB p65），核因子κBp50（NF‐κB p50）和环氧合酶2（COX‐2）的mRNA和蛋白表达水平。分别通过实时荧光定量PCR和蛋白质印迹。这项研究的结果表明，27-OHC处理可增加SH中TNF-α和iNOS的分泌并减少IL-10的分泌，上调TGF-β，NF-κBp65和p50的表达以及下调COX-2的表达‐SY5Y细胞。在C6细胞中，27-OHC处理导致IL-1β，IL-10，TNF-α和iNOS的分泌减少，以及TLR4和TGF-β的表达增加。这些结果表明27-OHC可能通过激活TGF-β/NF-κB信号传导途径对神经元造成炎性损害，并通过激活TLR4 /TGF-β信号传导对星形胶质细胞造成炎性损害，从而导致炎性细胞因子的后续释放。

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