INTRODUCTION Present investigation determines the beneficial effect of picroliv against lipopolysaccharide (LPS)-induced neuronal inflammation and injury. MATERIAL AND METHODS Neuronal injury was induced by LPS 250 µg/kg, i.p. for the period of one week, and picroliv 12.5 and 25 mg/kg was given i.p. 30 min prior to the administration of LPS for the duration of 12 days. The effect of picroliv was determined on the cognitive function by Morris water maze (MWM). Mediators of inflammation were estimated by using enzyme-linked immunosorbent assay (ELISA) and western blot, reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical analysis was done to determine the expressions of several proteins. RESULTS Data of the study reveal that picroliv ameliorates the reduced memory impairment and cognitive dysfunction in LPS-induced mice. Moreover, expressions of inflammatory protein and -amyloid protein and level of inflammatory mediators were found to be reduced in the picroliv-treated group as compared to the negative control group. Data of RT-PCR reveal that the gene of Toll-like receptor 4 (TLR-4), -synuclein, neurotrophic factor (BDNF) and interleukin-1 (IL-1) protein were also decreased in the picroliv-treated group as compared to the negative control group. In addition picroliv attenuates the altered level of nuclear factor-kB(p-NF-kB), amyloid- (A), -synuclein and glial fibrillary acidic protein (GFAP) positive cells in the brain of LPS-induced mice. CONCLUSIONS The report concludes that picroliv protects the neuroinflammation and injury in LPS-induced mice by regulating the inflammatory pathway.

中文翻译：

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Picroliv通过减弱TLR4 /NFκB途径对脂多糖诱导的认知功能障碍和神经炎症的保护作用。

引言目前的研究确定了吡咯夫对脂多糖（LPS）诱导的神经元炎症和损伤的有益作用。材料与方法LPS 250 µg / kg腹腔注射可诱发神经元损伤，持续1周，在LPS给药前30分钟腹腔注射12.5和25 mg / kg的吡咯利夫，持续12天。莫里斯水迷宫（MWM）确定了吡咯利夫对认知功能的影响。通过使用酶联免疫吸附测定（ELISA）和Western印迹，逆转录聚合酶链反应（RT-PCR）和免疫组织化学分析来确定几种蛋白质的表达，从而评估炎症的介导者。结果研究数据表明，吡咯夫可改善LPS诱导的小鼠的记忆力减退和认知功能障碍。而且，与吡咯烷酮处理组相比，与阴性对照组相比，炎性蛋白和β-淀粉样蛋白的表达以及炎性介质的水平降低。RT-PCR的数据显示，在吡咯夫利治疗后，Toll样受体4（TLR-4），γ-突触核蛋白，神经营养因子（BDNF）和白介素-1β（IL-1）的基因也减少了。与阴性对照组相比。此外，picroliv减弱了LPS诱导的小鼠大脑中核因子-kB（p-NF-kB），淀粉样β-（Aβ），γ-突触核蛋白和神经胶质原纤维酸性蛋白（GFAP）阳性细胞水平的改变。结论该报告得出结论，吡咯哌啶通过调节炎症途径来保护LPS诱导的小鼠的神经炎症和损伤。与阴性对照组相比，在吡咯夫利治疗组中，炎症蛋白和β-淀粉样蛋白的表达以及炎症介质的水平降低。RT-PCR的数据显示，在吡咯夫利治疗后，Toll样受体4（TLR-4），γ-突触核蛋白，神经营养因子（BDNF）和白介素-1β（IL-1）的基因也减少了。与阴性对照组相比。此外，picroliv减弱了LPS诱导的小鼠大脑中核因子-kB（p-NF-kB），淀粉样β-（Aβ），γ-突触核蛋白和神经胶质原纤维酸性蛋白（GFAP）阳性细胞水平的改变。结论该报告得出结论，吡咯哌啶通过调节炎症途径来保护LPS诱导的小鼠的神经炎症和损伤。与阴性对照组相比，在吡咯夫利治疗组中，炎症蛋白和β-淀粉样蛋白的表达以及炎症介质的水平降低。RT-PCR的数据显示，在吡咯夫利治疗后，Toll样受体4（TLR-4），γ-突触核蛋白，神经营养因子（BDNF）和白介素-1β（IL-1）的基因也减少了。与阴性对照组相比。此外，picroliv减弱了LPS诱导的小鼠大脑中核因子-kB（p-NF-kB），淀粉样β-（Aβ），γ-突触核蛋白和神经胶质原纤维酸性蛋白（GFAP）阳性细胞水平的改变。结论该报告得出结论，吡咯哌啶通过调节炎症途径来保护LPS诱导的小鼠的神经炎症和损伤。