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• W4285607714 abstract "Neuropathic pain (NP) is a chronic pain caused by somatosensory neuropathy or disease, and genistein (Gen) might be a potential drug for the treatment of NP. Therefore, this study aims to investigate the effect of Gen on lipopolysaccharide (LPS)-induced inflammatory injury of dorsal root ganglion neuron (DRGn) in rats and the possible molecular mechanism.The DRGn of 1-day-old juvenile rats were taken for isolation and culture. The DRGn in logarithmic growth phase were divided into a control group, a LPS group, a tubastatin hydrochloride (TSA)+LPS group, a Gen1+LPS group, a Gen2+LPS group, a Gen2+LPS+TSA group, a Gen2+pcDNA-histone deacetylase 6 (HDAC6)+LPS group, and a Gen2+pcDNA3.1+LPS group. The LPS group was treated with 1 μg/mL LPS for 24 h; the TSA+LPS group, the Gen1+LPS group, the Gen2+LPS group were treated with 5 μmol/L TSA, 5 μmol/L Gen, 10 μmol/L Gen respectively for 0.5 h, and then added 1 μg/mL LPS for 24 h; the Gen2+TSA+LPS group was treated with 10 μmol/L Gen and 5 μmol/L TSA for 0.5 h and then added 1 μg/mL LPS for 24 h; the Gen2+pcDNA-HDAC6+LPS group and the Gen2+pcDNA3.1+LPS group received 100 nmol/L pcDNA-HDAC6 and pcDNA3.1 plasmids respectively, and 24 h after transfection, 10 μmol/L Gen was pretreated for 0.5 h, and then added 1 μg/mL LPS for 24 h. Real-time RT-PCR was used to detect the HDAC6 mRNA expression in DRGn; CCK-8 method was used to detect cell viability of DRGn; flow cytometry was used to detect cell apoptosis of DRGn; ELISA was used to detect the levels of IL-1β, IL-6, and TNF-α in DRGn culture supernatant; Western blotting was used to detect the protein expression of HDAC6, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and NF-κB p65 in DRGn.Compared with the control group, the expression levels of HDAC6 mRNA and protein, the expression levels of TLR4 and MyD88 protein in DRGn of LPS group rats were significantly up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly increased, and the activity of DRGn was significantly decreased, the apoptosis rate was significantly increased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly increased (all P<0.05). Compared with the LPS group, the expression levels of HDAC6 mRNA and protein, TLR4 and MyD88 protein expression levels in DRGn of the TSA+LPS group, the Gen1+LPS group, the Gen2+LPS group and the Gen2+TSA+LPS group were significantly down-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly decreased, the activity of DRGn was significantly increased, the apoptosis rate was significantly decreased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly decreased (all P<0.05), and the above changes were most obvious in the Gen2+TSA+LPS group. Compared with the Gen2+LPS group, the expression levels of HDAC6 mRNA and protein, TLR4 and MyD88 protein expression levels in DRGn of the Gen2+pcDNA-HDAC6+LPS group were significantly up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly increased, the activity of DRGn was significantly decreased, and the apoptosis rate was significantly increased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly increased (all P<0.05).Gen can alleviate LPS-induced DRGn inflammatory injury in rats, which might be related to down-regulating the expression of HDAC6 and further inhibiting the activation of TLR4/MyD88/NF-κB signaling pathway.目的: 神经病理性疼痛(neuropathic pain，NP)是一种由躯体感觉神经病变或疾病引起的慢性疼痛，金雀异黄素(genistein，Gen)可能是治疗NP的潜在药物。因此，本研究旨在探讨Gen对脂多糖(lipopolysaccharide，LPS)诱导大鼠背根神经节神经元(dorsal root ganglion neuron，DRGn)炎性损伤的作用及其可能的分子机制。方法: 取出生 1 d的幼年大鼠进行DRGn的分离和培养。取对数生长期的DRGn，分为8组：对照组、LPS组、Tubastatin A盐酸盐(tubastatin A hydrochloride，TSA)+LPS组、Gen1+LPS组、Gen2+LPS组、Gen2+TSA+LPS组、Gen2+pcDNA-组蛋白脱乙酰化酶6(histone deacetylase 6，HDAC6)+LPS组、Gen2+pcDNA3.1+LPS组。LPS组给予1 μg/mL LPS处理24 h；TSA+LPS组、Gen1+LPS组、Gen2+LPS组给予5 μmol/L TSA、5 μmol/L Gen、10 μmol/L Gen预处理0.5 h后加入1 μg/mL LPS处理24 h；Gen2+TSA+LPS组给予10 μmol/L Gen和5 μmol/L TSA共同预处理0.5 h后加入1 μg/mL LPS处理24 h；Gen2+pcDNA-HDAC6+LPS组、Gen2+pcDNA3.1+LPS组将100 nmol/L pcDNA-HDAC6、pcDNA3.1质粒分别转染至DRGn，转染24 h后，给予10 μmol/L Gen预处理0.5 h，再加入1 μg/mL LPS处理24 h。采用real-time RT-PCR检测DRGn中HDAC6 mRNA的表达水平，CCK-8法检测DRGn活力，流式细胞术检测DRGn凋亡情况，ELISA检测DRGn培养上清液中IL-1β、IL-6、TNF-α水平；蛋白质印迹法检测DRGn中HDAC6、Toll样受体4(Toll-like receptor 4，TLR4)、髓样分化因子88(myeloid differentiation factor 88，MyD88)、NF-κB p65的蛋白质表达水平。结果: 与对照组相比，LPS组大鼠DRGn中HDAC6 mRNA和蛋白质的表达水平，TLR4和MyD88蛋白质表达水平均显著上调，p-NF-κB p65/NF-κB p65比值显著增加，DRGn活性显著降低且凋亡率显著升高，DRGn培养上清液中IL-1β、IL-6、TNF-α水平均显著升高(均P<0.05)。与LPS组相比，TSA+LPS组、Gen1+LPS组、Gen2+LPS组和Gen2+TSA+LPS组大鼠DRGn中HDAC6 mRNA和蛋白质的表达水平，TLR4和MyD88蛋白质表达水平均显著下调，p-NF-κB p65/NF-κB p65比值显著降低，DRGn活性显著升高且凋亡率显著降低，DRGn培养上清液中IL-1β、IL-6、TNF-α水平均显著降低(均P<0.05)，且Gen2+TSA+LPS组上述变化最明显。与Gen2+LPS组相比，Gen2+pcDNA-HDAC6+LPS组大鼠DRGn中HDAC6 mRNA和蛋白质的表达水平，TLR4和MyD88蛋白质表达水平均显著上调，p-NF-κB p65/NF-κB p65比值显著增加，DRGn活性显著降低且凋亡率显著升高，DRGn培养上清液中IL-1β、IL-6、TNF-α水平均显著升高(均P<0.05)。结论: Gen可减轻LPS诱导的大鼠DRGn炎性损伤，其作用机制可能与下调HDAC6的表达，进一步抑制TLR4/MyD88/NF-κB信号通路的激活有关。." @default.
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• W4285607714 date "2022-06-28" @default.
• W4285607714 modified "2023-10-16" @default.
• W4285607714 title "Genistein attenuates LPS-induced inflammatory injury of rat dorsal root ganglion neuron via down-regulating HDAC6." @default.
• W4285607714 doi "https://doi.org/10.11817/j.issn.1672-7347.2022.210428" @default.
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