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首页> 外文期刊>Neurochemical Research >Free Radical Generation by Neurons in Rat Model of Japanese Encephalitis
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Free Radical Generation by Neurons in Rat Model of Japanese Encephalitis

机译:神经元在日本脑炎大鼠模型中产生自由基

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摘要

Increased generation of free radicals resulting in brain injury is a feature of many viral infections. The present study has been undertaken to evaluate the level of free radicals in Japanese encephalitis. Twelve days old Wistar rats were inoculated intracerebrally with 3 × 106 pfu of JE virus and were sacrificed on 3, 6, 10, and 20 days post inoculation (dpi). The neuronal levels of reactive oxygen species (ROS), nitric oxide (NO), peroxinitrite (OONO−), necrotic and apoptotic cell population were estimated by flow cytometry. Hematoxylin-eosin staining was also performed. Maximum level of neuronal ROS and OONO− was observed on 6 dpi; however, NO levels peaked on 10 dpi. Free radical generation significantly declined on 20 dpi as compared to control. Apoptotic cell death gradually increased over the time. Neuronal shrinkage and necrosis was also observed. The results of our study indicate that free radicals increased in acute JE and declined at later stage, which may contribute to cell death.
机译:导致脑损伤的自由基产生的增加是许多病毒感染的特征。本研究已进行以评估日本脑炎中自由基的水平。在12天大的Wistar大鼠中,脑内接种3×10 6 pfu JE病毒,并在接种后(dpi)3、6、10和20天处死。通过流式细胞术评估了活性氧(ROS),一氧化氮(NO),过氧亚硝酸盐(OONO -),坏死和凋亡细胞群的神经元水平。还进行了苏木精-伊红染色。 6 dpi时观察到神经元ROS和OONO -的最大水平;但是,NO浓度在10 dpi时达到峰值。与对照组相比,自由基的产生在20 dpi时显着下降。随着时间的流逝,凋亡细胞死亡逐渐增加。还观察到神经元萎缩和坏死。我们的研究结果表明,急性脑脊髓炎的自由基增加,而在以后阶段则下降,这可能导致细胞死亡。

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