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狂犬病病毒糖蛋白 (RVG29) 连接的 microRNA-124 负载的聚合物纳米颗粒抑制帕金森病模型中的神经炎症。

Rabies virus glycoprotein (RVG29)-linked microRNA-124-loaded polymeric nanoparticles inhibit neuroinflammation in a Parkinson's disease model.

机构信息

Department of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.

Department of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.

出版信息

Int J Pharm. 2019 Aug 15;567:118449. doi: 10.1016/j.ijpharm.2019.118449. Epub 2019 Jun 18.

Abstract

In the present study, we have prepared microRNA(miR)-124-loaded Rabies virus glycoprotein (RVG)29 surface-conjugated polymeric nanoparticles (NPs) to improve neuroinflammation in Parkinson's disease (PD). We hypothesize that an increase in the intracellular concentration of miR-124 will result in a better prognosis for Parkinson's disease. Minimal toxicity for the RVG29 NPs was observed at concentrations <100 µg/mL, while the cell viability of cells treated with blank NPs at concentrations of 200 µg/mL markedly decreased, indicating the safety of the carrier system. Results showed that mRNA levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-6, significantly increased upon lipopolysaccharide (LPS) administration. However, the mRNA levels of these cytokines reflected those of the miR-NPs-treated control group, indicating the influence of miR-124 exposure. After transfection with miR-NPs, levels of pro-inflammatory cytokines and neuroprotective molecules were reduced and increased, respectively. Administration of LPS significantly increased the levels of mitogen activated protein kinase kinase kinase (MEKK)3 and P-P65 levels, while transfection with miR-NPs significantly reduced the expression of both MEKK3 and P-P65, reflecting that of the control. This research has revealed that miR-124 could target both the MEKK3 and nuclear factor kappa light chain enhancer of activated B cell (NF-Kb) pathways, while also reducing inflammatory cytokine levels. In addition, a 3-fold decrease in apoptosis was observed in miR-NP transfected cells. The exogenous delivery of miR-NPs significantly downregulated MEKK3 expression in animal studies, as outlined by immunohistochemical staining (IHC). Overall, miR-NPs have the potential to inhibit pro-inflammatory signaling and enhance neuroprotection in PD.

摘要

在本研究中,我们制备了装载 microRNA(miR)-124 的狂犬病病毒糖蛋白 (RVG)29 表面偶联聚合物纳米颗粒 (NPs),以改善帕金森病 (PD) 中的神经炎症。我们假设细胞内 miR-124 浓度的增加将导致帕金森病的预后更好。在浓度<100μg/mL 时,RVG29 NPs 的毒性最小,而空白 NPs 处理的细胞在浓度为 200μg/mL 时的细胞活力明显下降,表明载体系统的安全性。结果表明,在脂多糖 (LPS) 给药后,诱导型一氧化氮合酶 (iNOS)、肿瘤坏死因子-α (TNF-α) 和白细胞介素 (IL)-6 的 mRNA 水平显著增加。然而,这些细胞因子的 mRNA 水平反映了 miR-NPs 处理对照组的水平,表明 miR-124 暴露的影响。转染 miR-NPs 后,促炎细胞因子和神经保护分子的水平分别降低和增加。LPS 给药显著增加丝裂原激活蛋白激酶激酶激酶 (MEKK)3 和 P-P65 水平,而转染 miR-NPs 则显著降低 MEKK3 和 P-P65 的表达,反映了对照组的情况。这项研究表明,miR-124 可以靶向 MEKK3 和核因子 kappa 轻链增强子的激活 B 细胞 (NF-Kb) 途径,同时降低炎症细胞因子水平。此外,在 miR-NP 转染的细胞中观察到凋亡减少了 3 倍。免疫组织化学染色 (IHC) 表明,外源性递送 miR-NPs 可显著下调动物研究中 MEKK3 的表达。总的来说,miR-NPs 有可能抑制 PD 中的促炎信号并增强神经保护作用。

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