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植物类异戊二烯可减少脱髓鞘,并可恢复多发性硬化症的铜灰模型小鼠中受损的少突胶质细胞发生和神经发生。

Plant polyprenols reduce demyelination and recover impaired oligodendrogenesis and neurogenesis in the cuprizone murine model of multiple sclerosis.

机构信息

Laboratory of Neurobiology, Tomsk State University, Tomsk, Russian Federation.

Prenolica Limited (formerly Solagran Limited), Biotechnology Company, Melbourne, Victoria, Australia.

出版信息

Phytother Res. 2019 May;33(5):1363-1373. doi: 10.1002/ptr.6327. Epub 2019 Mar 12.

Abstract

Recent studies showed hepatoprotective, neuroprotective, and immunomodulatory properties of polyprenols isolated from the green verdure of Picea abies (L.) Karst. This study aimed to investigate effects of polyprenols on oligodendrogenesis, neurogenesis, and myelin content in the cuprizone demyelination model. Demyelination was induced by 0.5% cuprizone in CD-1 mice during 10 weeks. Nine cuprizone-treated animals received daily injections of polyprenols intraperitoneally at a dose of 12-mg/kg body weight during Weeks 6-10. Nine control animals and other nine cuprizone-treated received sham oil injections. At Week 10, brain sections were stained for myelin basic protein, neuro-glial antigen-2, and doublecortin to evaluate demyelination, oligodendrogenesis, and neurogenesis. Cuprizone administration caused a decrease in myelin basic protein in the corpus callosum, cortex, hippocampus, and the caudate putamen compared with the controls. Oligodendrogenesis was increased, and neurogenesis in the subventricular zone and the dentate gyrus of the hippocampus was decreased in the cuprizone-treated group compared with the controls. Mice treated with cuprizone and polyprenols did not show significant demyelination and differences in oligodendrogenesis and neurogenesis as compared with the controls. Our results suggest that polyprenols can halt demyelination, restore impaired neurogenesis, and mitigate reactive overproduction of oligodendrocytes caused by cuprizone neurotoxicity.

摘要

最近的研究表明,从云杉绿芽中分离出的多萜醇具有护肝、护脑和免疫调节特性。本研究旨在探讨多萜醇对寡树突胶质细胞发生、神经发生和髓鞘含量的影响,在脱髓鞘模型中环己酮诱导。在 10 周内,用 0.5%的环己酮诱导 CD-1 小鼠脱髓鞘。9 只环己酮处理的动物在第 6-10 周期间每天接受 12mg/kg 体重的多萜醇腹腔注射。9 只对照动物和另外 9 只环己酮处理的动物接受假油注射。第 10 周时,对大脑切片进行髓鞘碱性蛋白、神经胶质抗原-2 和双皮质素染色,以评估脱髓鞘、少突胶质细胞发生和神经发生。与对照组相比,环己酮处理导致胼胝体、皮质、海马和尾状核中的髓鞘碱性蛋白减少。与对照组相比,环己酮处理组少突胶质细胞发生增加,而室下区和海马齿状回的神经发生减少。与对照组相比,用环己酮和多萜醇处理的小鼠未表现出明显的脱髓鞘和少突胶质细胞发生和神经发生的差异。我们的结果表明,多萜醇可以阻止脱髓鞘,恢复受损的神经发生,并减轻环己酮神经毒性引起的反应性少突胶质细胞过度增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af38/6594192/0a00dc657afc/PTR-33-1363-g001.jpg

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