Rutin Supplementation in the Diet has Protective Effects Against Toxicant-Induced Hippocampal Injury by Suppression of Microglial Activation and Pro-Inflammatory Cytokines

Rutin Supplementation in the Diet has Protective Effects Against Toxicant-Induced Hippocampal Injury by Suppression of Microglial Activation and Pro-Inflammatory Cytokines
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DOI:
10.1007/s10571-008-9344-4
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发表时间:
2009-06-01
影响因子:
4
通讯作者:
Imai, Hideki
Imai, Hideki
中科院分区:
医学3区
文献类型:
--
作者:
Koda, Tomoko;Kuroda, Yoshiki;Imai, Hideki

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目的芦丁是类黄酮中的一种,对健康有许多有益的作用。先前,我们发现芦丁对三甲基锡(TMT)诱导的大鼠记忆功能障碍具有保护作用。本研究旨在探讨芦丁对tmt诱导的大鼠海马损伤的保护作用及其时间过程。方法4周龄雄性SD大鼠在实验期间分别饲喂含或不含芦丁(0.75%)的饲料,6周龄时分别给予单剂量TMT (8.5 mg/kg b.w., p.o)或载药。分别于TMT给药后5、10、20天处死大鼠,进行海马组织和分子检查。结果补充芦丁可抑制TMT诱导的海马锥体神经元数量减少。TMT诱导的反应性小胶质细胞标志物和促炎细胞因子mRNA表达水平上调在TMT给药后10或20天被补充芦丁逆转。结论芦丁对tmt诱导的空间记忆损伤的神经保护作用可能与其抑制小胶质细胞的激活以及通过海马神经营养因子参与突触的形成有关。
Aims Rutin is one of the flavonoids that has many beneficial effects on the health. Previously, we showed that rutin has a protective effect on trimethyltin (TMT)-induced memory dysfunction in rats. The aim of this study was to investigate the protective effects of rutin on TMT-induced hippocampal injury and the time course profiles of these effects in rats. Methods Four-week-old male Sprague-Dawley (SD) rats were fed chow with or without rutin (0.75%) during the experimental period and were administered with a single dose of TMT (8.5 mg/kg b.w., p.o.) or vehicle at 6 weeks of age. The rats were sacrificed 5, 10, or 20 days after the TMT administration and then histological and molecular examinations of the hippocampus were performed. Results Rutin supplementation suppressed the TMT-induced decrease in the number of hippocampal pyramidal neurons 20 days after TMT administration. The TMT-induced up-regulation of the mRNA expression levels of reactive microglia marker and pro-inflammatory cytokines were reversed by rutin supplementation 10 or 20 days after the TMT administration. Conclusions These results suggested that the neuroprotective effect of rutin on TMT-induced spatial memory impairment could be attributable to its inhibitory effect against microglial activation and its role in synapse formation via neurotrophic factors in the hippocampus.